A Systematic Review of Dementia Research Priorities

Affiliations.

  • 1 Social Ageing (SAGE) Futures Lab, School of Arts and Humanities, Edith Cowan University, Perth, WA, Australia.
  • 2 Centre for Research in Aged Care, School of Nursing and Midwifery, Edith Cowan University, Perth, WA, Australia.
  • PMID: 38337159
  • DOI: 10.1177/08919887241232647

Introduction: Patient involvement is a critical component of dementia research priority-setting exercises to ensure that research benefits are relevant and acceptable to those who need the most. This systematic review synthesises research priorities and preferences identified by people living with dementia and their caregivers.

Methods: Guided by Joanna Briggs Institute methodology, and Preferred Reporting Items for Systematic Reviews and Meta-Analyses framework, we conducted a systematic search in five electronic databases: CINAHL, Medline, PsycINFO, Web of Science and Scopus. The reference lists of the included studies were also manually searched. We combined quantitative and qualitative data for synthesis and descriptive thematic analysis.

Results: Eleven studies were included in this review. Findings are grouped into four main categories: Increase in knowledge, education, and awareness; Determining the cause; Sustainability of care; and Cure of dementia and related conditions.

Conclusion: There is a need to respond to the stigma associated with dementia, which limits access to care and the quality of life for both people living with dementia and their caregivers. We need to work on changing public, private and workplace attitudes about dementia and encourage supporting and participating in dementia research. Future research should involve people living with dementia and their primary caregivers from culturally and linguistically diverse communities in priority-setting exercises.

Keywords: alzheimer’s disease; behavioural disturbances; cognitive decline; dementia; geriatrics; health services research.

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Population Studies & Health Disparities

Scientists continue to expand research on how the combined effects of genes, lifestyle, environment, and general health may determine a person’s risk for dementia. Through NIH-funded population studies, researchers are helping to identify and address dementia-related health disparities based on race and ethnicity, sex, education, and socioeconomic status.

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NIH population studies reveal new links to brain changes associated with Alzheimer’s and related dementias

Nih funding helps to unravel links between dementia and covid-19 and other infectious diseases, nih-funded population studies analyze genetic risk factors for alzheimer’s.

  • Health disparities negatively affect dementia diagnosis and care 

Program update: An NIH genomics data program enables population studies around the world

A physical therapist working with a senior.

Dementia-related brain changes can start a decade or more before a person experiences symptoms and may result from a complex interplay among abnormal tau and beta-amyloid proteins and several other factors. Recent results from the following NIH-funded studies shed more light on how brain health in general affects the risk of developing Alzheimer’s disease:

  • People who have Alzheimer’s often have multiple types of brain lesions , and this is more common in people with worse symptoms of dementia. Data from 5,272 individuals from the National Alzheimer’s Coordinating Center showed that most people with Alzheimer’s have both brain changes that are specific to the disease, such as tau tangles and amyloid plaques in the case of Alzheimer’s, and brain changes more commonly associated with other related dementias.
  • People who have a stroke that is moderate or severe or who have multiple strokes may have a significantly higher risk of dementia than people who have had a mild stroke . According to data from more than 1,000 participants in the NIH-funded Atherosclerosis Risk in Communities cohort study, people who have two or more moderate or severe strokes are almost seven times more likely to develop dementia than people who have not had a stroke. Having a stroke before age 75 can also significantly raise the risk of dementia. The findings emphasize the importance of stroke prevention as a means of mitigating dementia risk.
  • People who develop mental disorders early in life have an increased risk of all types of dementia and of developing dementia at a younger age . These findings, obtained from an analysis of hospitalization records for 1.7 million individuals from New Zealand’s national health system, suggest that effectively treating mental disorders earlier in life may lower the risk of developing dementia.

Back to top .

NIH is playing a critical role in COVID-19 response efforts concerning older adults, who are at a much greater risk of severe illness and death from this infectious disease. In 2021, an NIA-funded study based on the electronic health records of about 61.9 million U.S. adults from all 50 states showed that people with any type of dementia have twice the risk of getting COVID-19 than people without dementia do. People with dementia are also more likely to have severe or fatal cases of COVID-19, and this risk is even higher for Black people living with dementia.

Current NIA and National Institute of Neurological Disorders and Stroke (NINDS) studies are expanding our knowledge of how COVID-19 affects brain health in older adults with and without dementia, including the effects of prolonged symptoms of COVID-19, technically called post-acute sequelae of SARS-CoV-2 infection (PASC) and more commonly referred to as “Long COVID.” In 2021, NIH launched the Researching COVID to Enhance Recovery (RECOVER) Initiative , a national-level, patient-centered study of national scale with thousands of diverse participants from across the lifespan, that will include research into the disease’s effects on cognition, cognitive decline, and dementia.

NIA has also funded a number of research projects on whether viral infections and other microbial pathogens contribute to Alzheimer’s. NIA held a workshop on the infectious etiology of Alzheimer’s in 2021. Additionally, in a study partially funded by NIA, researchers discovered a link between mononucleosis and Alzheimer’s .

Infographic showing how Covid-19 affects older adults. For more details, read the Progress Report linked at the top of the page.

The NIA Alzheimer’s Disease Genetics Portfolio supports research to identify genes that raise or lower the risk of Alzheimer’s and to understand how these genes influence the processes in cells that lead to the disease.

To date, scientists have identified more than 70 genetic regions associated with Alzheimer’s.

The APOE4 gene variant has been found to be one of the most significant genetic risk factors for Alzheimer’s; however, the link between APOE4 and Alzheimer’s risk differs between racial and ethnic groups. For example, an NIA-supported study published in 2022 found that the APOE4 variant is not linked to dementia-related brain changes or cognitive impairment in American Indians .

APOE4 is linked with Alzheimer’s risk in people of African ancestry, but not to the same degree as in people of European ancestry . A recent study helps explain why this may be the case. It found that people of European ancestry have higher levels of APOE4 protein in their brains than people of African ancestry . The authors think that the region around the APOE4 gene differs by ancestry and controls how much APOE protein is made. These findings and the critical nuances in APOE4 and disease risk by population group underscore the importance of studying Alzheimer’s in diverse populations.

  • In people of European ancestry, an Alzheimer’s polygenic risk score (an estimate of a person’s risk of Alzheimer’s based on many known genetic risk factors) gives an accurate estimate of the risk for the disease. However, the risk score, which was produced from studies involving mostly people of European ancestry, was not a good predictor in people of African ancestry. This highlights the importance of more diverse population studies in order to determine specific genetic risk factors across racial and ethnic groups and create polygenic risk scores that apply to people of non-European ancestry.
  • Specific regions of DNA may control the levels of proteins linked to neurological disorders in various tissue types. Proteins that are controlled by the same regions of DNA may work together in a biological process to raise or lower a person’s risk of dementia .
  • A new technique examines how changes to a gene will affect the 3D structure of proteins made from that gene , which can help scientists identify rare gene variants linked to Alzheimer’s. Using the new method, researchers identified new variants of four genes, two of which ( TREM2 and SORL1 ) are known to be linked to the disease. The other two are CSF1R , which has been suggested but not confirmed as contributing to Alzheimer’s, and EXOC3L4 , a novel Alzheimer’s risk gene. Because changes to a protein’s structure can interfere with its function, studying these gene variants can help researchers understand the roles these genes play in raising the risk of dementia and how to use this information to develop new therapeutic targets.

Health disparities negatively affect dementia diagnosis and care

Following specific priorities identified using its Health Disparities Research Framework , NIA has awarded grants to explore the environmental, sociocultural, behavioral, and biological determinants of health disparities related to aging. In 2021, findings from these studies underscored the following.

  • Among people who participate in research studies on Alzheimer’s, Black participants with symptoms of the disease are less likely than White participants to have received a clinical diagnosis of Alzheimer’s than White participants . Additionally, Black participants with Alzheimer’s have more risk factors for the disease and more severe symptoms than White participants do. Another study showed that racial disparities in dementia prevalence between Black and White individuals did not improve from 2000 to 2016 .
  • Although researchers found that more people living with dementia received a dementia diagnosis from 2006 to 2013, the condition is still underdiagnosed in Black and Hispanic individuals , highlighting the need for improved diagnostic methods among racial and ethnic minority populations. In this study, researchers compared the number of people diagnosed with dementia using three sources of data: cognitive tests, detailed neuropsychological tests, and diagnosis codes from Medicare claims. They found that over the years, the difference in estimated prevalence of dementia from these three data sources has lessened, showing that dementia underdiagnosis is decreasing overall.
  • Compared with older adults living in urban areas, older adults who live in rural communities are less likely to receive a clinical diagnosis of Alzheimer’s or a related dementia, are often diagnosed at later stages of dementia, and have a shorter survival time after diagnosis . Increased measures to promote dementia screening in rural areas could help address these disparities.
  • People who do not have easy access to primary care have a higher risk of cognitive impairment . Improving health care access may help lower the risk of cognitive decline and dementia.

Infographic showing Alzheimer's health disparities between men and women. For more details, read the Progress Report linked at the top of the page.

NIH established the Alzheimer’s Disease Sequencing Project (ADSP) in 2012 to sequence and analyze genomic data from large Alzheimer’s studies conducted worldwide. The overarching goals in 2022 are to:

  • Identify new gene variants that increase the risk of Alzheimer’s and related dementias
  • Identify gene variants that protect against dementia
  • Provide insights into why some people with known risk factor genes do not develop dementia symptoms
  • Identify potential avenues for therapeutic approaches to prevent or treat dementias
  • Examine all of these factors in diverse populations

ADSP data have revealed several potential genetic risk or protective factors for Alzheimer’s. For example, in 2021, researchers found that although genome-wide association studies and family-based studies often identify different sets of Alzheimer’s-related genes, many of these genes function in the same or similar processes in brain cells . This strengthens the evidence for the involvement of specific underlying processes in the disease. To understand how these and other gene variants lead to Alzheimer’s, NIA funded six projects in 2021 through the ADSP Functional Genomics Consortium , which will utilize a multipronged team science strategy and large-scale, high-throughput approaches.

Also in 2021, ADSP researchers launched two important initiatives:

  • The Phenotype Harmonization Consortium is a major effort to combine and organize clinical data from all ADSP studies and share these data with the research community, with the goal of stimulating new drug development. The consortium’s efforts will improve the usability of ADSP data and facilitate research to identify well-targeted therapeutic approaches for Alzheimer’s and related dementias.
  • The ADSP Follow-Up Study 2.0: The Diverse Population Initiative will expand ADSP data to represent a more diverse population. Current ADSP data are derived mostly from White clinical study participants, and results based on these data might not be an accurate reflection of the genetic factors linked to Alzheimer’s in all populations. The new follow-up study will help researchers identify not only common gene variants but also rare variants that may play an important role in Alzheimer’s and related dementias.

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  • Published: 12 February 2024

Plasma proteomic profiles predict future dementia in healthy adults

  • Yu Guo 1   na1 ,
  • Jia You   ORCID: orcid.org/0000-0002-7079-8041 1 , 2   na1 ,
  • Yi Zhang 1   na1 ,
  • Wei-Shi Liu 1 ,
  • Yu-Yuan Huang 1 ,
  • Ya-Ru Zhang 1 ,
  • Wei Zhang 2 ,
  • Qiang Dong   ORCID: orcid.org/0000-0002-3874-0130 1 ,
  • Jian-Feng Feng   ORCID: orcid.org/0000-0001-5987-2258 2 , 3 ,
  • Wei Cheng   ORCID: orcid.org/0000-0003-1118-1743 1 , 2 , 3 &
  • Jin-Tai Yu   ORCID: orcid.org/0000-0002-2532-383X 1  

Nature Aging volume  4 ,  pages 247–260 ( 2024 ) Cite this article

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  • Neurodegeneration
  • Predictive markers

The advent of proteomics offers an unprecedented opportunity to predict dementia onset. We examined this in data from 52,645 adults without dementia in the UK Biobank, with 1,417 incident cases and a follow-up time of 14.1 years. Of 1,463 plasma proteins, GFAP, NEFL, GDF15 and LTBP2 consistently associated most with incident all-cause dementia (ACD), Alzheimer’s disease (AD) and vascular dementia (VaD), and ranked high in protein importance ordering. Combining GFAP (or GDF15) with demographics produced desirable predictions for ACD (area under the curve (AUC) = 0.891) and AD (AUC = 0.872) (or VaD (AUC = 0.912)). This was also true when predicting over 10-year ACD, AD and VaD. Individuals with higher GFAP levels were 2.32 times more likely to develop dementia. Notably, GFAP and LTBP2 were highly specific for dementia prediction. GFAP and NEFL began to change at least 10 years before dementia diagnosis. Our findings strongly highlight GFAP as an optimal biomarker for dementia prediction, even more than 10 years before the diagnosis, with implications for screening people at high risk for dementia and for early intervention.

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case studies for dementia

Data availability

The data used in the present study are available from UK Biobank with restrictions applied. Data were used under license and are thus not publicly available. Access to the UK Biobank data can be requested through a standard protocol ( https://www.ukbiobank.ac.uk/register-apply/ ). Data used in this study are available in the UK Biobank under application number 19542. All data supporting the findings described in this manuscript are available in the article and in the supplementary materials and from the corresponding author upon request. Source data are provided with this paper.

Code availability

All software used in this study is publicly available. The code used in this study can be accessed at https://github.com/jasonHKU0907/DementiaProteomicPrediction .

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Acknowledgements

We thank all the participants and researchers from the UK Biobank. W.C. was funded by National Key Research and Development Program of China (grant no. 2023YFC3605400). J.T.-Y. was funded by grants from the Science and Technology Innovation 2030 Major Projects (grant no. 2022ZD0211600), National Natural Science Foundation of China (grant nos. 82071201, 92249305), Research Start-up Fund of Huashan Hospital (grant no. 2022QD002) and Excellence 2025 Talent Cultivation Program at Fudan University (grant no. 3030277001). J.F.-F. was funded by National Key R&D Program of China (grant nos. 2018YFC1312904, 2019YFA0709502), Shanghai Municipal Science and Technology Major Project (grant no. 2018SHZDZX01) and the 111 Project (no. B18015). J.Y. was funded by Shanghai Pujiang Talent Program (grant no. 23PJD006). The funders had no role in study design, data collection and analysis; decision to publish or preparation of the manuscript. Further, we would like to thank the support from the ZHANGJIANG LAB, Tianqiao and Chrissy Chen Institute, and the State Key Laboratory of Neurobiology and Frontiers Center for Brain Science of Ministry of Education, Fudan University.

Author information

These authors contributed equally: Yu Guo, Jia You, Yi Zhang.

Authors and Affiliations

Department of Neurology and National Center for Neurological Disorders, Huashan Hospital, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Shanghai Medical College, Fudan University, Shanghai, China

Yu Guo, Jia You, Yi Zhang, Wei-Shi Liu, Yu-Yuan Huang, Ya-Ru Zhang, Qiang Dong, Wei Cheng & Jin-Tai Yu

Institute of Science and Technology for Brain-inspired Intelligence, Fudan University, Shanghai, China

Jia You, Wei Zhang, Jian-Feng Feng & Wei Cheng

Key Laboratory of Computational Neuroscience and Brain-inspired Intelligence, Fudan University, Ministry of Education, Shanghai, China

Jian-Feng Feng & Wei Cheng

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J.-T.Y. undertook conceptualization and design of the study, interpretation of the data and revision of the manuscript. Y.G., J.Y. and Y.Z. collected, analyzed and interpreted the data, and drafted and revised the manuscript. J.-F.F., W.C. and J.-T.Y. were responsible for funding, administrative, technical or material support. All authors carried out revision of the manuscript. All authors had full access to all the study data and accepted responsibility for submitting it for publication.

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Correspondence to Jian-Feng Feng , Wei Cheng or Jin-Tai Yu .

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Extended data

Extended data fig. 1 flowchart for participants’ enrollment..

From the UK Biobank cohort, we excluded individuals with dementia at baseline or with self-reported dementia and those who did not undergo plasma proteomic assay. The remaining participants were classified based on their first reported years of ACD or AD or VaD after baseline. Abbreviations: ACD, all-cause dementia; AD, Alzheimer’s disease; VaD, vascular dementia.

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Supplementary Figs. 1–6.

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Guo, Y., You, J., Zhang, Y. et al. Plasma proteomic profiles predict future dementia in healthy adults. Nat Aging 4 , 247–260 (2024). https://doi.org/10.1038/s43587-023-00565-0

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DOI : https://doi.org/10.1038/s43587-023-00565-0

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Case studies

These three case studies help you to consider different situations that people with dementia face. They are:

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  • Joan , an older woman, who lives alone and has just been diagnosed with dementia

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  • An ecogram showing who is involved
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  • v.13(18); 2021 Sep 30

Helicobacter pylori infection and risk for developing dementia: an evidence-based meta-analysis of case-control and cohort studies

Nan-yang liu.

1 Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, China

Jia-Hui Sun

2 Beijing University of Traditional Chinese Medicine, Beijing, China

Xue-Fan Jiang

3 Wangjing Hospital, China Academy of Chinese Medical Sciences, Beijing, China

Associated Data

Background: Infection with multiple pathogens may play a key role in the pathogenesis of dementia. Whether Helicobacter pylori ( H. pylori ) infection is associated causally with dementia is controversial.

Objective: We conduct a meta-analysis of case-control and cohort studies on the association between H. pylori infection and the risk for all-cause and Alzheimer’s disease (AD) dementia.

Methods: Two independent reviewers searched the PubMed, Cochrane Library, and Embase databases with English language restrictions from the date of conception to September 18, 2020. The primary analysis was as follows: the exposure variable was H. pylori infection, and the outcome was incident all-cause and AD dementia. Pooled odds ratios (OR), relative risk (RR), and corresponding 95% confidence intervals (CI) were obtained using the fixed-or random-effect model. Forest plots were generated to summarize the results.

Results: Ten studies involving 96,561 participants were included in the meta-analysis: 5 case-control studies and 5 cohort studies. The overall pooled cohort studies showed a significant positive association between H. pylori infection and all-cause dementia with pooled RR of 1.36 (95% CI, 1.11-1.67). There was no association between H. pylori infection and risk for developing AD: RR of 1.33 (95% CI, 0.86-2.05) in cohort studies, and OR of 1.72 (95% CI, 0.97-3.04) in case-control studies. Significant heterogeneity was showed in each comparison group.

Conclusion: This meta-analysis supports a positive association between H. pylori infection and the risk of all-cause dementia, but not AD dementia. Due to the interference of confounding factors, randomized controlled trials are needed to prove their causality.

INTRODUCTION

Dementia is a serious social and medical problem that affects the health of people older than 65 years worldwide. The most common types of dementia were Alzheimer’s disease (AD) and vascular dementia, accounting for 60%-70% and 30%, respectively. Currently, there are more than 50 million people with dementia worldwide, and this number will increase to 152 million by 2050 [ 1 ]. The 2019 Alzheimer’s disease facts and figures in the United States showed that between 2000 and 2017, deaths resulting from stroke, heart disease, and prostate cancer decreased, whereas reported deaths from AD increased 145% [ 1 ]. Such a situation is not optimistic in Asia. Recent data show that the number of dementia in China accounts for approximately 25% of the total number of dementia in the world [ 2 ].

The identified risk factors for dementia include sociodemographic structure (age, gender, low education level) and family history. In addition, infections, diabetes, hypertension, and stroke can also contribute to the occurrence of dementia [ 3 ]. Emerging data have demonstrated that infection with several important pathogens may be a hazard factor for cognitive impairment, dementia, and AD in particular [ 4 ]. Among them, Helicobacter pylori ( H. pylori ) is the most interesting for researchers [ 5 , 6 ]. H. pylori , the only microbial species currently known to survive in the human stomach, was successfully isolated from the gastric mucosa of patients with chronic active gastritis for the first time in 1984 [ 7 ]. Infection occurs mainly in childhood and generally survives in the body. However, most people are asymptomatic during infection [ 8 ]. Chronic H. pylori infection is a direct inducement of chronic gastritis, peptic ulcers, and gastric cancer. Interestingly, H. pylori has also been identified as a risk factor for non-gastrointestinal diseases, such as neurodegenerative diseases, including all-cause and AD dementia [ 9 – 11 ].

Previous evidence suggests H. pylori infection as a driver of cognitive decline. The potential link between H. pylori infection and dementia have been investigated by several population-based case-control and cohort studies, but the results were inconsistent. Although a previous meta-analysis that combined several observational studies have reported a statistically significant association between H. pylori infection and all-cause dementia, the evidence was limited to inappropriate statistical methods [ 12 ]. And one of the studies even included patients with mild cognitive impairment rather than the dementia, leading to unconvincing evidence. Therefore, the purpose of this study was to conduct a systematic review and meta-analysis of case-control and cohort studies to understand the association between H. pylori infection and the risk of developing all-cause and AD dementia.

Literature search

A total of 269 records were identified from all databases. After excluding 30 duplicate analysis, 239 records were filtered by reading the title and abstract. A total of 189 items were excluded due to irrelevant topics. We screened the full text of the remaining 50 studies and identified 10 studies that met the inclusion criteria of the meta-analysis, including 5 case-control studies and 5 cohort studies. The detailed PRISMA flowchart describing the literature search process is presented in Figure 1 .

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Flow diagram of the literature selection process.

Study characteristics and quality

The ten studies, published between 2003 and 2018, varied in design, study population, sample size, outcome variables, and methods used to determine H. pylori infection. With respect to the countries that conducted these studies, one of them was conducted in the United States [ 13 ], six in Europe [ 14 – 19 ], two in China [ 20 , 21 ], and one in Japan [ 22 ]. The sample sizes of the studies ranged from 61 to 83965. Of five case-control studies, four studies used nondementia control groups [ 16 , 19 , 20 , 22 ], and one study used an iron deficiency anemic control group [ 18 ]. Nine studies reported AD [ 13 – 16 , 18 – 22 ], whereas 6 reported all-cause dementia [ 13 – 17 , 21 ]. The follow-up time for the cohort study ranged from 3 to 20 years. The average age of the study samples in each group was between 59.3 and 78.5 years old. The identification of H. pylori infection involved serum IgG antibodies, rapid urine tests, and gastric mucosal histology. Six studies detected IgG antibodies in the serum [ 13 – 15 , 17 , 19 , 20 ], and one study measured histology together with serum IgG antibodies [ 16 ]. One study was based on codes in the International Classification of Diseases 9th edition from national registries [ 21 ], one used histology [ 18 ] and one used rapid urine test [ 22 ]. Two of ten studies did not adjust for confounding factors [ 14 , 16 ]. In the Newcastle-Ottawa scale assessment, all studies received a high score of ≥ 6 stars, indicating that the quality of the literature was reliable ( Table 1 ).

AD, Alzheimer’s Disease; DSM-III-R, Statistical Manual of Mental Disorders–3rd Edition Revised; FRSSD, Functional Rating Scale for Symptoms of Delirium; ICD-9-CM, International Classification of Diseases 9, Ninth Revision, Clinical Modification; ICD-10, International Classification of Diseases 10; MMSE, Mini Mental State Examination; M(SD), Mean (standard deviation); N, Number of population; NA, not available; NINCDS–ADRDA, National Institute of Neurological Disorders and Stroke and Alzheimer’s Disease and Related Disorders Association; NI, Neuropsychiatric Inventory.

Meta-analysis of the association between H. pylori infection and all-cause dementia in cohort study

Five cohort studies investigated the correlation between H. pylori infection and all-cause dementia, including two retrospective and three prospective. Figure 2 shows the results of pooled RR with a random-effects model. Four studies demonstrated a significant positive association and the RR for the association ranged from 1.03 to 1.70. Overall, the pooled results indicated that H. pylori infection participants had a considerably risk of developing all-cause dementia compared to those negative for H. pylori (RR = 1.36; 95% CI = 1.11 - 1.67), with significant heterogeneity ( I 2 = 64.4%, P = 0.024). Sensitivity analysis was assessed by removing each study in sequence and re-analysing the data shows that the study of Fani et al. has an impact on the results ( Supplementary Figure 1 ). Interestingly, the heterogeneity decreased to 0% after excluding this study, while the effect estimates increased (RR = 1.50; 95% CI = 1.31-1.73) ( Supplementary Figure 2 ).

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Forest plot presents the association between Helicobacter pylori infection and the risk of all-cause dementia in cohort study.

Meta-analysis of the association between H. pylori infection and AD dementia in cohort study

Figure 3 shows the results of pooled RRs with a random-effect model of AD dementia. Four cohort studies reported the association between H. pylori infection and AD dementia, whereas two studies reported a significant positive association. The pooled RRs of developing AD after H. pylori infection in cohort studies were 1.33 (95% CI, 0.86-2.05), demonstrating that there is no causal association. Sensitivity analysis was used to assess the robustness of the results, which resulted in almost identical risk estimates. ( Supplementary Figure 3 ).

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Object name is aging-13-203571-g003.jpg

Forest plot presents the association between Helicobacter pylori infection and the risk of Alzheimer’s disease in cohort study.

Meta-analysis of the association between H. pylori infection and AD dementia in case-control study

Five case-control studies described the connection between H. pylori infection and AD dementia. The pooled results of the random-effect model demonstrate that there is no correlation between H. pylori infection and the incidence of AD (OR=1.72; 95% CI=0.97-3.04) ( Figure 4 ), with significant heterogeneity ( I 2 = 67.2%, P = 0.016). Evaluating the robustness of the results by removing each study in sequence and reanalyzing the data did not lead to remarkable difference in the results ( Supplementary Figure 4 ). However, excluding the study of Kountouras et al. reduced the heterogeneity to 19.1% ( Supplementary Figure 5 ).

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Object name is aging-13-203571-g004.jpg

Forest plot presents the association between Helicobacter pylori infection and the risk of Alzheimer’s disease in case-control study.

Publication bias

The Begg rank correlation test and Egger linear regression test documented no evidence of publication bias among studies between H. pylori infection and the risk of all-cause and AD dementia (all P < 0.05).

Previous researches have been performed to examine the association between H. pylori infection and various cognitive outcomes, including all-cause and AD dementia. However, the association is not fully understood [ 23 – 26 ]. Our results are limited to observational studies suggest that H. pylori infection may be an independent risk factor for all-cause dementia, but not for AD. In fact, the average follow-up time for these cohort studies is 3 to 20 years. This large time interval between the two diseases further confirms the assumption that H. pylori infection is an independent risk factor for all-cause dementia.

Positive correlation between H. pylori infection and all-cause dementia was found in the previous meta-analysis, which is consistent with our findings. However, the authors pooled different study types results in significant heterogeneity, which reduced the credibility of the evidence. In addition, they included a study diagnosed as mild cognitive impairment rather than AD or all-cause dementia. Our evidence is based on independent cohort and case-control studies showing that H. pylori infection can lead to subsequent all-cause dementia, which makes the evidence more credible.

Several neurological diseases related to H. pylori infection have been reported so far, such as AD, stroke [ 27 ], Parkinson’s disease [ 28 ] and multiple sclerosis [ 29 ]. In some disease, only the correlation is explained without a clear interpretation of the pathogenic mechanism, which makes this a very interesting and controversial topic. However, for some infected groups, the association is so powerful and the pathogenic mechanism is so obvious that guidelines for the treatment of H. pylori infection recommend that eradication treatment should be carried out in this case. Here, we focus on the connection among H. pylori infection and dementia. Multiple lines of evidence have suggested that infection with H. pylori is a key driver of AD [ 30 – 32 ]. One study reported beneficial effects on cognitive and functional status parameters of patients with AD after H. pylori eradication [ 33 ]. Another study showed a higher 5-year survival rate after H. pylori eradication in AD patients [ 34 ]. However, our study found no evidence supporting the connection between H. pylori infection and AD susceptibility, which is inconsistent with those reports. Inconsistent results may be limited by the ethnicity of the included population, study design, and H. pylori identification method.

The potential physiological mechanisms involved in H. pylori infection and dementia are uncertain, but several candidate mechanisms have been identified. One possible explanation is the neuroinflammation hypothesis that involves a central event triggering neurodegeneration, including AD [ 35 , 36 ]. Previous researches have demonstrated that H. pylori infection may cause damage to the blood-brain barrier and induce neurological diseases by releasing various inflammatory mediators, for instance, cytokines and chemokines [ 37 , 38 ]. H. pylori infection may also indirectly affect the brain by releasing multiple cytokines, for example, tumor necrosis factor-α and interleukin-6, maintaining cerebrospinal fluid inflammatory factors at a high level and thus inducing neuroinflammation [ 39 , 40 ]. In another study, MNK-28 human gastric cells were incubated with H. pylori peptide, and activated genes were monitored [ 41 ]. The results showed that 77 genes were modulated by the H. pylori peptide, of which 65 are identified in the AlzBase database and contain the characteristics of AD. Additionally, a large proportion of modulated genes (30 out of 77) pertains to the inflammation pathway.

The other explanation is that chronic gastritis induced by H. pylori infection can cause vitamin B12 and folate malabsorption, which leads to the accumulation of folate 5-methyltetrahydrofolate and homocysteine [ 42 – 44 ]. Increased homocysteine can trigger endothelial atherosclerotic thrombotic disease and AD damage [ 45 – 47 ]. Multiple lines of evidence have confirmed this hypothesis. For example, hyperhomocysteinemia was demonstrated to be a strong independent factor in the progress of dementia [ 48 ]. Another study also revealed that homocysteine levels are associated with cardiovascular disease and dementia in the context of chronic gastritis (including H. pylori causality) [ 49 ]. The authors believe that vitamin B12, folate levels and suffering from atrophic gastritis are crucial determinants of homocysteine levels but are not associated with dementia. In addition, B12 deficiency resulting from by H. pylori infection may be related to activation of tau and β-amyloid (Aβ) deposition [ 50 ]. Recent evidence suggests that vitamin B 12 inhibits Aβ 42 aggregation in a concentration-dependent manner and protects amyloid-induced cytotoxicity of human neuronal cell lines [ 51 ]. An adequate supply of vitamin B12 appears to be essential to prevent cognitive decline and prevent the progression of AD [ 52 ].

It noticeable that observational studies cannot confirm causality. Despite that, our report meets the causality of some Hill criteria. First, there is a distinct time relationship in the cohort study. H. pylori infection preceded the occurrence of dementia in all preliminary studies. Given that H. pylori is acquired during childhood, the infection precedes the onset of dementia. Second, the positive associations between different studies and populations were extensively consistent. Third, as mentioned above, the hypothesis that H. pylori infection predisposes to dementia is biologically plausible.

Sources of heterogeneity

Significant heterogeneity was discovered in the current systematic review and meta-analysis due to clinical and methodological diversity, such as the differences in characteristics of demographic, determination of H. pylori infection and adjustment of confounding factors. The study of Fani et al. likely contributed to the heterogeneity in the exploration of the relationship between H. pylori infection and all-cause dementia [ 15 ]. In fact, the association in this study was significantly reduced compared with that in other studies, which may be due to the use of different diagnostic criteria. The pooled RR mildly increased after excluding this study (from 1.36 to 1.50), but there is no evidence of heterogeneity observed in the remaining researches ( I 2 =0%, P =0.95). Additionally, the study of Kountouras et al. may be the main cause of heterogeneity due to a very strong association (OR=8.4). One possible reason accounting for this strong association may be that patients with anemia were included as the control group. Interestingly, previous evidence has suggested that patients with pernicious anemia were protected from infection with H. pylori [ 53 ].

The potential limitations of current research warrant consideration. First, a direct causal relationship between H. pylori infection and AD or all-cause dementia risk cannot be determined because observational studies were included. Therefore, the results should be interpreted cautiously. Second, as a meta-analysis of observational researches published in English, publication bias may be possible. We conducted a comprehensive retrieval of the literature to eliminate publication bias as much as possible. Third, another possible restriction of the present systematic review and meta-analysis was the use of various detection methods for H. pylori infection. Fourth, substantial heterogeneity was found among studies. Although the main source of heterogeneity was detected through sensitivity analysis, we still cannot exclude the probability that residual confounding could influence the results. Finally, un-controlled or un-measurable risk factors in the study may produce biases. Although conventional risk factors have been adjusted in some studies, the possibility of residual confounding factors that increase the risk of dementia cannot be excluded.

Suggestions for further study

Based on our findings, several issues need to be considered. First, is there any causal relationship between H. pylori infection and AD dementia? To answer this question, the interval between the two diseases and adequate control of confounding factors should be assessed. Second, what is the exact mechanism by which H. pylori increase the risk of all-cause dementia? Neuroinflammation and hyperhomocysteinemia may provide some ideas. Third, can the eradication of H. pylori prevent or delay the development of dementia? Further studies are needed, including rigorously-designed clinical trials to tackle these issues to better understand this association and provide persuasive evidence for clinical practice in dementia prevention.

CONCLUSIONS

In conclusion, this systematic review and meta-analysis suggest that H. pylori infection may be associated with an increased risk of all-cause dementia, but not AD dementia. Future research on the pathogenic mechanism between the two diseases may lead to the development of novel therapies. The clinical implications lie in maintaining vigilance against dementia in elderly patients infected with H. pylori , and early detection and timely medical treatment for H. pylori patients through a multidisciplinary approach.

MATERIALS AND METHODS

Search strategy and study selection.

This systematic review and meta-analysis were conducted based on the Meta-analysis Of Observational Studies in Epidemiology (MOOSE) [ 51 ]. Two independent reviewers (N-YL and J-HS) searched PubMed, the Cochrane Library, and Embase databases with English language restrictions from the inception to July 10, 2019. The search terms were “ Helicobacter pylori/H. pylori or Campylobacter pylori/C. pylori ” and at least one of the following: “dementia or Alzheimer’s disease”. Two independent researchers (N-YL and HL) evaluated the article abstracts determined by the initial search to ensure qualified study, and then obtained and evaluated all potentially relevant articles in detail. References from the latest reviews were also searched. Eligible studies were randomized controlled trials, controlled clinical trials, cohort studies, and case–control studies on the relationship between adult H. pylori infection and dementia. The study set the following criteria: (1) interest in exposure to H. pylori infection (yes or not); (2) interest in all-cause and AD dementia; (3) studies including relative risk (RR), hazard ratio (HR), or odds ratio (OR), and their corresponding 95% confidence intervals (CIs) and P -value (or calculated data). Intervention studies, case reports, case series, duplicate reports, letters to editors, comments, and author responses were excluded.

Data extraction and quality assessment

The standardized data form was used to extract the following information: author name, year of publication, country, period and follow-up time, reference materials, study design and population, sample size, H. pylori detection method, outcome variables, and statistical adjustment of confounding factors. The RR, HR, OR, and the corresponding CIs were extracted for each study (or calculated from reported data). We used the Newcastle-ottawa scale recommended by the Cochrane Collaboration to evaluate the methodological quality of the eligible studies [ 52 ]. The evaluation content includes three parts: selection, comparability, and exposure/outcome. There are 8 items in this scale with a total score of 9. Quality assessments and data extraction were performed by two researchers (X-FJ and HL), and any discrepancies that existed were resolved by discussion.

Statistical analysis

Stata version 12.0 (Stata Corp LP, College Station, Texas) was used to calculate the pooled ORs, HRs, RRs, and 95% CIs. Forest plots were generated to summarize the results. Heterogeneity χ 2 test and I 2 index were used to assess the heterogeneity between the eligible studies. I 2 ≤50% were deemed to have little heterogeneity; I 2 >50% were considered to have considerable heterogeneity. When heterogeneity cannot readily be interpreted, we incorporate it into a random-effect model [ 53 ]. Instead, we used a fixed-effect model. Potential sources of heterogeneity were identified by sensitivity analysis. Publication bias was evaluated using the Begg rank correlation test or Egger linear regression test.

Supplementary Material

Supplementary figures, acknowledgments.

We would like to thank all the authors who contributed to the systematic review.

Abbreviations

AUTHOR CONTRIBUTIONS: Conceived and designed the experiments: HL. Performed the experiments: N-YL and J-HS. Analyzed the data: HL. Contributed reagents/materials/analysis tools: N-YL and X-FJ. Wrote the paper: N-YL. Read, reviewed and approved the final manuscript: N-YL, J-HS, X-FJ, and HL. Had primary responsibility for final content: HL. All authors read and approved the final manuscript.

CONFLICTS OF INTEREST: The authors declare that they have no conflicts of interest.

FUNDING: This work was supported by the China National Science and Technology Major Project for “Essential new drug research and development” (No.2018ZX09301038-003). The funding source had no role in the study.

Scientists Found 5 Factors to Improve Brain Health and Lower Dementia Risk

Doctors say they may even be more helpful than medicine.

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  • New research links certain healthy habits to a sharper brain as you age.
  • The study followed participants for more than two decades.
  • Doctors say these are good habits to follow for brain and overall health.

There’s a general recipe for living well that includes regular physical activity, eating a healthy diet, and avoiding smoking. Now, new research finds five factors that can also help support brain health and sharp thinking as you age,

The researchers found a direct link between healthy lifestyle habits and a lowered risk of cognitive decline as the participants got older—that was true, even in people who had hallmark signs of developing Alzheimer’s disease or dementia . Lead study author Klodian Dhana, M.D., Ph.D., an assistant professor of geriatrics and palliative medicine at the Rush Institute for Healthy Aging, says his team wanted to see if certain factors could influence whether someone develops Alzheimer’s or dementia. “As individuals age, there is a progressive accumulation of dementia-related brain pathologies,” he says. However, not everyone goes on to develop dementia, despite these changes in the brain. The goal of the study, Dr. Dhana says, was to see if lifestyle factors would make a difference in how likely someone is to develop dementia.

Here’s what Dr. Dhana and his team discovered.

Factors to improve brain health

The study participants were labeled as having a low-risk or healthy lifestyle if they did the following:

  • No smoking.
  • Doing moderate to vigorous exercise for at least 150 minutes a week.
  • Limit alcohol use to one drink a day for women and two drinks a day for men.
  • Engage in brain-stimulating activities, like reading, playing games, and visiting museums.
  • Follow a variation of the MIND diet.

Study participants received a healthy lifestyle score within these areas and, the healthier they were, the better their brain health. The researchers found that for every one-point increase in the healthy lifestyle score, the lower the amount of beta-amyloid plaques (hallmarks of Alzheimer’s disease ) and the higher their score on cognitive tests that looked at factors like memory and attention span.

An editorial that was published alongside the study pointed out that the benefits of following these healthy lifestyle factors were still there, regardless of whether the study participants had signs of dementia and Alzheimer’s disease in their brains.

Why are these habits good for the brain?

At baseline, these lifestyle factors and habits are known to be good for you. “Following a healthy lifestyle is good for the brain,” says Amit Sachdev, M.D., M.S., medical director in the Department of Neurology at Michigan State University.

These factors in particular “have been investigated and shown to be associated with slower cognitive decline and a lower risk of dementia,” Dr. Dhana says.

While plant-based diets have been linked to healthier brains, the MIND diet is a specific kind of plant-based diet. It incorporates several elements of the Mediterranean diet , like plenty of fruits, vegetables, nuts, beans, olive oil, and whole grains, explains Jessica Cording, M.S., R.D., author of The Little Book of Game-Changers: 50 Healthy Habits For Managing Stress & Anxiety .

“Previous studies on similar diet patterns have shown that this style of eating is very rich in polyphenols, which are powerful plant compounds that have been shown to have neuroprotective properties,” Cording says. “That’s a big piece of the puzzle.” The foods featured in this diet can help tamp down on bodily inflammation and promote good gut and heart health, she points out.

That diet, along with regular exercise, limiting alcohol use, and avoiding smoking is good for the cardiovascular system, Cording says. “What’s good for the heart and blood vessels is generally good for the brain—we have tons of blood vessels in the brain,” she says.

Clifford Segil, D.O. , a neurologist at Providence Saint John’s Health Center in Santa Monica, CA., agrees. “A healthy lifestyle increases your heart health and brain health,” he says. “A healthy heart can only help your brain.”

Research has also found that doing mentally stimulating activities is linked with a lowered risk of developing dementia. “The thing I most often recommend to patients for their brain health is structured cognitive exercise,” Dr. Segil says. “That can mean taking a class at a junior college. With muscles, if you don’t use it, you lose it. The same is true of your brain.”

Dr. Segil stresses the importance of healthy lifestyle habits for brain health, noting that he sees patients do better after making lifestyle tweaks than they do taking certain medications to lower the risk of cognitive decline.

Overall, Dr. Dhana says the lifestyle factors laid out in his study may help provide cognitive benefits over time. But, if you’re concerned about your own risk of dementia or have a family history of the disease, he recommends seeing a doctor for personalized recommendations.

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Dementia case study with questions and answers

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Dementia case study with questions and answers

Common dementia exam questions for medical finals, OSCEs and MRCP PACES

The case below illustrates the key features in the assessment of a patient with dementia or undiagnosed memory decline. It works through history, examination and investigations – click on the plus symbols to see the answers to each question

Part 1: Mavis

  • Mavis is an 84-year old lady, referred to you in the memory clinic for assessment of memory impairment. She attends in the company of her son and daughter-in-law.
  • On the pre-clinic questionnaire her son has reported a severe deterioration in all aspects of her cognition over the past 12 months.
  • The patient herself acknowledges that there have been memory problems, but feels it is just her short term memory that is an issue.

Question 1.

  • To begin the history, start broadly. Build rapport and establish both the patient’s view on memory impairment (if any) and the family’s (or other collateral history).
  • Patient’s (and collateral) view of memory decline
  • Biographical history
  • Objective view of memory decline (e.g. knowledge of current affairs)
  • Impact of memory decline on day-to-day living and hobbies
  • Social history, including safety and driving
  • General medical history (especially medications)
  • See below for details on these…

Question 2.

  • Is it for everything or are specific details missed out/glossed over?
  • Try to pin down specific details (e.g. names of people/places).
  • At what time in chronological order do things start to get hazy?

Question 3.

  • If under 12 years this will lead to additional point being awarded on some cognitive tests
  • Ask about long term memories, e.g. wedding day or different jobs
  • Then move on to more recent memories, e.g. last holiday

Question 4.

  • If your patient watches the news/read newspapers on a regular basis, ask them to recount the headlines from the past few days.
  • Be sure to look for specifics to prevent your patient masking memory deficiencies with broad statements. For example: “The government are incompetent, aren’t they?!” should be clarified by pinning down exactly why they are incompetent, for example: “Jeremy Hunt”.
  • If they like to read, can they recall plotlines from current books or items from magazines?
  • If they watch TV, can they recount recent plot lines from soaps, or formats of quiz shows?

Question 5.

  • Ask about hobbies and other daily activities, and whether or not these have declined recently.
  • If your patient no longer participates in a particular hobby, find out why: is it as a result of a physical impairment (e.g. arthritis making cooking difficult), or as the result of a loss of interest/ability to complete tasks (e.g. no longer able to complete crosswords/puzzles).
  • Once you have a good idea of the memory decline itself, begin to ask about other features. Including a social and general medical history.

Question 6.

  • Review their social history and current set-up, and also subjective assessments from both patient and family over whether or not the current arrangements are safe and sustainable as they are.
  • Previous and ongoing alcohol intake
  • Smoking history
  • Still driving (and if so, how safe that is considered to be from collateral history)
  • Who else is at home
  • Any package of care
  • Upstairs/downstairs living
  • Meal arrangements (and whether weight is being sustained).
  • Of all these issues, that of driving is perhaps one of the most important, as any ultimate diagnosis of dementia must be informed (by law) to both the DVLA and also the patient’s insurers. If you feel they are still safe to drive despite the diagnosis, you may be asked to provide a report to the DVLA to support this viewpoint.

Now perform a more generalised history, to include past medical history and – more importantly – a drug history.

Question 7.

  • Oxybutynin, commonly used in primary care for overactive bladder (anticholinergic side effects)
  • Also see how the medications are given (e.g. Dossett box)
  • Are lots of full packets found around the house?

Part 2: The History

On taking a history you have found:

  • Mavis was able to give a moderately detailed biographical history, but struggled with details extending as far back as the location of her wedding, and also her main jobs throughout her life.
  • After prompting from her family, she was able to supply more information, but it was not always entirely accurate.
  • Her main hobby was knitting, and it was noted that she had been able to successfully knit a bobble hat for her great-grand child as recently as last month, although it had taken her considerably longer to complete than it might have done a few years previously, and it was a comparatively basic design compared to what she has been able to create previously.
  • She has a few children living in the area, who would frequently pop in with shopping, but there had been times when they arrived to find that she was packed and in her coat, stating that she was “just getting ready to go home again”.
  • She had been helping occasionally with the school run, but then a couple of weekends ago she had called up one of her sons – just before she was due to drive over for Sunday lunch – and said that she could not remember how to drive to his house.
  • Ever since then, they had confiscated her keys to make sure she couldn’t drive. Although she liked to read the paper every day, she could not recall any recent major news events.  Before proceeding to examine her, you note that the GP referral letter has stated that her dementia screen investigations have been completed.

Question 8.

  • Raised WCC suggests infection as a cause of acute confusion
  • Uraemia and other electrolyte disturbances can cause a persistent confusion.
  • Again, to help rule out acute infection/inflammatory conditions
  • Liver failure can cause hyperammonaemia, which can cause a persistent confusion.
  • Hyper- or hypothyroidism can cause confusion.
  • B12 deficiency is an easily missed and reversible cause of dementia.
  • This looks for space occupying lesions/hydrocephalus which may cause confusion.
  • This can also help to determine the degree of any vascular component of an ultimately diagnosed dementia.

Part 3: Examination

  • With the exception of age-related involutional changes on the CT head (noted to have minimal white matter changes/small vessel disease), all the dementia screen bloods are reassuring.
  • You next decide to perform a physical examination of Mavis.

Question 9.

  • Important physical findings that are of particular relevance to dementia, are looking for other diseases that may have an effect on cognition.
  • To look for evidence of stroke – unlikely in this case given the CT head
  • Gait (shuffling) and limb movements (tremor, rigidity, bradykinesia)
  • Affect is also important here and may also point to underlying depression
  • Pay attention to vertical gaze palsy, as in the context of Parkinsonism this may represent a Parkinson plus condition (e.g. progressive supranuclear palsy).
  • It is also useful to look at observations including blood pressure (may be overmedicated and at risk of falls from syncope) and postural blood pressure (again, may indicate overmedication but is also associated with Parkinson plus syndromes e.g. MSA)

Part 4: Cognitive Testing

  • On examination she is alert and well, mobilising independently around the clinic waiting room area.  A neurological examination was normal throughout, and there were no other major pathologies found on a general examination.
  • You now proceed to cognitive testing:

Question 10.

  • Click here for details on the MOCA
  • Click here for details on the MMSE
  • Click here for details on the CLOX test

Part 5: Diagnosis

  • Mavis scores 14/30 on a MOCA, losing marks throughout multiple domains of cognition.

Question 11.

  • Given the progressive nature of symptoms described by the family, the impairment over multiple domains on cognitive testing, and the impact on daily living that this is starting to have (e.g. packing and getting ready to leave her own home, mistakenly believing she is somewhere else), coupled with the results from her dementia screen, this is most likely an Alzheimer’s type dementia .

Question 12.

  • You should proceed by establishing whether or not Mavis would like to be given a formal diagnosis, and if so, explain the above.
  • You should review her lying and standing BP and ECG, and – if these give no contraindications – suggest a trial of treatment with an acetylcholinesterase inhibitor, such as donepezil.
  • It is important to note the potential side effects – the most distressing of which are related to issues of incontinence.
  • If available, put her in touch with support groups
  • Given the history of forgetting routes before even getting into the care, advise the patient that she should stop driving and that they need to inform the DVLA of this (for now, we will skip over the depravation of liberty issues that the premature confiscation of keys performed by the family has caused…)
  • The GP should be informed of the new diagnosis, and if there are concerns over safety, review by social services for potential support should be arranged.
  • Follow-up is advisable over the next few months to see whether the trial of treatment has been beneficial, and whether side effects have been well-tolerated.

Now click here to learn more about dementia

Perfect revision for medical students, finals, osces and mrcp paces, …or  click here to learn about the diagnosis and management of delirium.

IMAGES

  1. dementia case study analysis

    case studies for dementia

  2. (PDF) Case management for dementia in primary health care: A systematic

    case studies for dementia

  3. Providing the best possible support to Dementia patients and their

    case studies for dementia

  4. Case Studies in Dementia, Vol 2: Common and Uncommon Presentations

    case studies for dementia

  5. Case study on dementia

    case studies for dementia

  6. Quantitative Imaging for Dementia

    case studies for dementia

VIDEO

  1. Is This True For Dementia Care?

  2. LIVING WITH DEMENTIA EP. 30

  3. LIVING WITH DEMENTIA EP. 19

  4. Ask a Specialist: WHAT IS DEMENTIA?

COMMENTS

  1. Case Report of a 63-Year-Old Patient With Alzheimer Disease ...

    CASE REPORT The patient was referred to our specialty memory clinic at the age of 58 with a 2-year history of repetitiveness, memory loss, and executive function loss. Magnetic resonance imaging scan at age 58 revealed mild generalized cortical atrophy. She is white with 2 years of postsecondary education.

  2. Case 41-2020: A 62-Year-Old Man with Memory Loss and Odd Behavior

    2 Citing Articles Presentation of Case Dr. David L. Perez: A 62-year-old, left-handed man was seen in the memory disorders clinic of this hospital because of memory loss, personality changes, and...

  3. A Case Report of a 37-Year-Old Alzheimer's Disease Patient with

    CASE A 37-year old male patient visited outpatient clinic, with complaints of gradual cognitive decline which had started 3 years earlier. Working as an industrial researcher, he started to make serious calculation mistakes that made him quit the job and began working as a manager in a company.

  4. Dementia prevention, intervention, and care: 2020 report of the

    Overall, a growing body of evidence supports the nine potentially modifiable risk factors for dementia modelled by the 2017 Lancet Commission on dementia prevention, intervention, and care: less education, hypertension, hearing impairment, smoking, obesity, depression, physical inactivity, diabetes, and low social contact.

  5. Medical Management and Patient Care

    Case management. Legal and financial advice. Workforce development focused on training families and caregivers. Program effectiveness At one year, the quality of care provided by the program as measured by nationally accepted quality measures for dementia was exceedingly high — 92% compared to a benchmark of 38%.

  6. Clinical Trials for Alzheimer's & Dementia

    Individuals with dementia, caregivers and healthy volunteers are all needed to participate in clinical studies focused on Alzheimer's and other dementias. About Clinical Trials Without clinical trials, there can be no better treatments, no prevention and no cure for Alzheimer's disease.

  7. Case Studies in Dementia

    This collection of case studies from around the world illustrates both common and unusual causes of dementia, emphasizing clinical reasoning, integrative thinking and problem-solving skills. Each case consists of a clinical history, examination findings and special investigations, followed by diagnosis and discussion.

  8. Case Studies in Dementia

    Case Studies in Dementia Common and Uncommon Presentations Search within full text Get access Edited by Pedro Rosa-Neto, McGill University, Montréal, Serge Gauthier, McGill University, Montréal Publisher: Cambridge University Press Online publication date: January 2021 Print publication year: 2021 Online ISBN: 9781316941294 DOI:

  9. A Systematic Review of Dementia Research Priorities

    Introduction: Patient involvement is a critical component of dementia research priority-setting exercises to ensure that research benefits are relevant and acceptable to those who need the most. This systematic review synthesises research priorities and preferences identified by people living with dementia and their caregivers.

  10. The Enigma of Lewy Body Dementia: a Case Report

    We reviewed a case of a 71-year-old patient whose clinical presentation gradually occurred with complex visual hallucinations, atypical extrapyramidal motor symptoms, fluctuating cognitive impairments with delirious episodes, and oscillating syncope. Depressive mood, impaired daily functioning and sensitivity to antipsychotics were also noted.

  11. Case 10

    Chapter Information Case Studies in Dementia Common and Uncommon Presentations , pp. 44 - 48 DOI: https://doi.org/10.1017/9781316941294.011 Publisher: Cambridge University Press Print publication year: 2021 Access options Get access to the full version of this content by using one of the access options below.

  12. Population Studies & Health Disparities

    NIH-funded population studies analyze genetic risk factors for Alzheimer's. The NIA Alzheimer's Disease Genetics Portfolio supports research to identify genes that raise or lower the risk of Alzheimer's and to understand how these genes influence the processes in cells that lead to the disease.. To date, scientists have identified more than 70 genetic regions associated with Alzheimer's.

  13. Plasma proteomic profiles predict future dementia in healthy adults

    This study included 52,645 adults without dementia at baseline, with a median age of 58 years, ... To achieve this, a nested case-control study design was carried out.

  14. Phenocopy behavioral variant frontotemporal dementia: A case study

    Abstract. Objective: Behavioral variant frontotemporal dementia (bvFTD) is a neurodegenerative condition characterized by progressive changes in behavior, cognition, and day-to-day functioning. Progression of the disease usually leads to death 3-5 years after diagnosis. However, there are reports of individuals who are initially diagnosed with bvFTD but fail to progress.

  15. Dementia prevention, intervention, and care: 2020 report of the

    Overall, a growing body of evidence supports the nine potentially modifiable risk factors for dementia modelled by the 2017 Lancet Commission on dementia prevention, intervention, and care: less education, hypertension, hearing impairment, smoking, obesity, depression, physical inactivity, diabetes, and low social contact.

  16. PDF Dementia Through Clinical Cases

    Clinical Cases Fireside Chat - Alzheimer's Association 7th Annual Kansas Education Conference on Dementia Ryan W. Schroeder, PsyD, LP, ABPP-CN Board Certified Clinical Neuropsychologist Primary cognitive change: -Difficulty learning and remembering new information -Able to remember old information Common behavior changes:

  17. Case Studies in Dementia: Volume 1

    Dementia is amongst the greatest challenges facing the medical profession as the population ages. Accurate diagnosis is essential as many rarer forms of the disease are treatable if recognized early. This collection of case studies from around the world illustrates both common and unusual causes of dementia, emphasizing clinical reasoning, integrative thinking and problem-solving skills.

  18. Case studies

    Each case study contains: A vignette setting out the situation An ecogram showing who is involved An assessment which gives essential information about what is happening and the social worker's conclusion A care and support plan which says what actions will be taken to achieve outcomes

  19. Vascular Cognitive Impairment (Case 26)

    Serge Gauthier Chapter Get access Cite Summary An 85-year-old woman with hypertension and hyperlipidemia presented with gradual and progressive cognitive impairment for more than 2 years, involving cognitive domains of memory, executive function, visuospatial and mood.

  20. Helicobacter pylori infection and risk for developing dementia: an

    Background: Infection with multiple pathogens may play a key role in the pathogenesis of dementia. Whether Helicobacter pylori (H. pylori) infection is associated causally with dementia is controversial.Objective: We conduct a meta-analysis of case-control and cohort studies on the association between H. pylori infection and the risk for all-cause and Alzheimer's disease (AD) dementia.

  21. These 5 Habits Improve Brain Health and Lower Dementia Risk: Study

    Lead study author Klodian Dhana, M.D., Ph.D., an assistant professor of geriatrics and palliative medicine at the Rush Institute for Healthy Aging, says his team wanted to see if certain factors ...

  22. PDF Case Studies in Dementia

    A catalog record for this publication is available from the British Library. Library of Congress Cataloging-in-Publication Data. Case studies in dementia : common and uncommon presentations / edited by Serge Gauthier, Pedro Rosa-Neto. p. ; cm. Includes bibliographical references and index. ISBN 978--521-18830-2 (pbk.) 1. Dementia-Case ...

  23. Portraits of People With Dementia: Three Case Studies of Creating

    Portraits of People With Dementia: Three Case Studies of Creating Portraits - Gemma Webster, Deborah Fels, 2013. Who would be involved in the collection process will depend fully on the family and current situation and structure of the person with dementia. The information included in the Portraits was all very different and unique in some ...

  24. Case Studies in Dementia

    This collection of case studies from around the world illustrates both common and unusual causes of dementia, emphasizing clinical reasoning, integrative thinking and problem-solving skills. Each case consists of a clinical history, examination findings and special investigations, followed by diagnosis and discussion.

  25. Dementia case study with questions and answers

    Question 1. What are the key features to address in a dementia history? Question 2. What specific features of memory decline do you want know? Question 3. What are the key parts of a biographical history? Question 4. What are the best way to get a current overview of memory? Question 5. How do you measure the impact of memory loss on daily life?

  26. Case Studies in Dementia: Common and Uncommon Presentations (Case

    Covering the spectrum of cognitive decline in aging using illustrative cases, from mild impairment to dementia, this set of case studies offers a wide-ranging guide for trainees and clinicians. This second volume includes updated research diagnostic criteria and details of new imaging technology, including novel biomarkers such as PET amyloid ...

  27. Dementia Following Stroke (Case 25)

    Case Studies in Dementia Common and Uncommon Presentations , pp. 112 - 115 DOI: https://doi.org/10.1017/9781316941294.026 Publisher: Cambridge University Press Print publication year: 2021 Access options Get access to the full version of this content by using one of the access options below.