INTRODUCTION The prevalence of frailty at population level is unclear. We examined this in population-based studies, investigating sources of heterogeneity. METHODS PubMed, Embase, CINAHL and Cochrane Library databases were searched for observational population-level studies published between 1 January 1998 and 1 April 2020, including individuals aged ≥50 years, identified using any frailty measure. Prevalence estimates were extracted independently, assessed for bias and analysed using a random-effects model. RESULTS In total, 240 studies reporting 265 prevalence proportions from 62 countries and territories, representing 1,755,497 participants, were included. Pooled prevalence in studies using physical frailty measures was 12% (95% CI = 11-13%; n = 178), compared with 24% (95% CI = 22-26%; n = 71) for the deficit accumulation model (those using a frailty index, FI). For pre-frailty, this was 46% (95% CI = 45-48%; n = 147) and 49% (95% CI = 46-52%; n = 29), respectively. For physical frailty, the prevalence was higher among females, 15% (95% CI = 14-17%; n = 142), than males, 11% (95% CI = 10-12%; n = 144). For studies using a FI, the prevalence was also higher in females, 29% (95% CI = 24-35%; n = 34) versus 20% (95% CI = 16-24%; n = 34), for males. These values were similar for pre-frailty. Prevalence increased according to the minimum age at study inclusion. Analysing only data from nationally representative studies gave a frailty prevalence of 7% (95% CI = 5-9%; n = 46) for physical frailty and 24% (95% CI = 22-26%; n = 44) for FIs. CONCLUSIONS Population-level frailty prevalence varied by classification and sex. Data were heterogenous and limited, particularly from nationally representative studies making the interpretation of differences by geographic region challenging. Common methodological approaches to gathering data are required to improve the accuracy of population-level prevalence estimates. PROTOCOL REGISTRATION PROSPERO-CRD42018105431.

Prevalence of frailty in 62 countries across the world: a systematic review and meta-analysis of population-level studies

Defects in mitochondrial oxidative phosphorylation have frequently been associated with Alzheimer9s disease (AD), and both inherited and somatic mtDNA mutations have been reported in certain AD cases. To determine whether mtDNA mutations contribute more generally to the etiology of AD, we have investigated the sequence of the mtDNA control region (CR) from AD brains for possible disease-causing mutations. Sixty-five percent of the AD brains harbored the T414G mutation, whereas this mutation was absent from all controls. Moreover, cloning and sequencing of the mtDNA CR from patient and control brains revealed that all AD brains had an average 63% increase in heteroplasmic mtDNA CR mutations and that AD brains from patients 80 years and older had a 130% increase in heteroplasmic CR mutations. In addition, these mutations preferentially altered known mtDNA regulatory elements. Certain AD brains harbored the disease-specific CR mutations T414C and T477C, and several AD brains between 74 and 83 years of age harbored the CR mutations T477C, T146C, and T195C, at levels up to 70–80% heteroplasmy. AD patient brains also had an average 50% reduction in the mtDNA L-strand ND6 transcript and in the mtDNA/nuclear DNA ratio. Because reduced ND6 mRNA and mtDNA copy numbers would reduce brain oxidative phosphorylation, these CR mutations could account for some of the mitochondrial defects observed in AD.

https://www.pnas.org/content/pnas/101/29/10726.full.pdf

Alzheimer's brains harbor somatic mtDNA control-region mutations that suppress mitochondrial transcription and replication

https://www.cell.com/trends/neurosciences/pdf/S0166-2236(00)01584-8.pdf

Energetics in the pathogenesis of neurodegenerative diseases.

Purpose: This systematic review examines research and practical applications of the World Health Organization Disability Assessment Schedule (WHODAS 2.0) as a basis for establishing specific criter...

World Health Organization disability assessment schedule 2.0: An international systematic review

The mitochondrial theory of aging proposes that mitochondrial DNA (mtDNA) accumulates mutations with age, and that these mutations contribute to physiological decline in aging and degenerative diseases. Although a great deal of indirect evidence supports this hypothesis, the aggregate burden of mtDNA mutations, particularly point mutations, has not been systematically quantified in aging or neurodegenerative disorders. Therefore, we directly assessed the aggregate burden of brain mtDNA point mutations in 17 subjects with Alzheimer's disease (AD), 10 elderly control subjects and 14 younger control subjects, using a PCR-cloning-sequencing strategy. We found that brain mtDNA from elderly subjects had a higher aggregate burden of mutations than brain mtDNA from younger subjects. The average aggregate mutational burden in elderly subjects was 2 x 10(-4) mutations/bp. The bulk of these mutations were individually rare point mutations, 60% of which changed an amino acid. Control experiments ensure that these results were not due to artifacts arising from PCR error, mistaken identification of nuclear pseudogenes or ex vivo oxidation. Cytochrome oxidase activity correlated negatively with increasing mutational burden. These findings significantly bolster the mitochondrial theory of aging.

High aggregate burden of somatic mtDNA point mutations in aging and Alzheimer’s disease brain

This is a research paper for the Wanless Social Care Review, the outcome of which was the report, Securing Good Care for Older People (King's Fund, 2006).

/pdf/compression-or-expansion-of-disability-forecasting-future-2ojbfsfiqq.pdf

Compression or expansion of disability?: forecasting future disability levels under changing patterns of diseases.

The genetic factors that predispose to Alzheimer's disease (AD) are heterogeneous. Two recent reports have suggested that a mitochondrial DNA mutation within the tRNAGln gene, located at position 4336, may be a risk factor for AD, as it was found in 10/256 (3.9%) cases with AD confirmed by necropsy. Although low prevalences of this mutation were detected in non-demented subjects in both of these studies, the controls were not carefully matched with the AD cases. We have investigated the frequency of this mutation in two community based elderly cohorts in Cambridgeshire, who have participated in longitudinal studies of cognitive function. The 4336 mitochondrial mutation was detected in 8/ 443 people examined. These people were found to be non-demented at ages 74, 81, 84, 86, 89, 90, 91, and 102 years, in contrast to the previously described cases whose onset of dementia occurred between 60 and 76 years (mean 68). Accordingly, we believe that this mitochondrial variant is not a high penetrance mutation which predisposes to dementia before the age of 76 years.

https://jmg.bmj.com/content/jmedgenet/33/12/1002.full.pdf

The tRNA(Gln) 4336 mitochondrial DNA variant is not a high penetrance mutation which predisposes to dementia before the age of 75 years.

White matter lesions in an unselected cohort of the elderly: Prevalence, relation to other patholgies and risk factors

Background There is relative little information about the prevalence and risk factors of co-morbid anxiety and depression in later life. These disorders are often associated with worse response to treatment than either condition alone, and researching its epidemiology in diverse settings is vital to policy makers. We therefore investigated the co-occurrence of anxiety and depressive syndromes among older adults living in developing countries and measured the separate and joint effect of these two disorders on levels of associated disability. Method The 10/66 study carried out cross-cultural surveys of all residents aged 65 or over (n=15 021) in 11 sites in seven countries (China, India, Cuba, Dominican Republic, Venezuela, Mexico and Peru). Anxiety was measured by using the Geriatric Mental State Examination (GMS) and the AGECAT diagnostic system. Depression was assessed according to ICD-10 and EURO-DEP criteria. Disability was measured by using the WHO-Disablement Assessment Scale Version II (WHODAS-II). Negative binomial regression models (ZINBs) were used to investigate the association between common mental disorders and disability. Results Co-morbid anxiety and depression was high (range %: 14.4–26.8) in the Latin American and Indian sites. Gender, socio-economic status, urbanicity and physical co-morbidities were associated with the different co-morbid states. Having both disorders was linked to higher disability scores than having anxiety or depression alone. Conclusions Given the close association of co-morbid anxiety and depression with disability, new policies to improve prevention, recognition and treatment will be needed to adapt to ageing populations and their mental health needs.

https://jech.bmj.com/content/jech/65/Suppl_1/A369.2.full.pdf

P2-536 Co-occurrence of anxiety and depression among older adults in low and middle-income countries: findings from the 10/66 study

Microglial activation in white matter of the ageing brain

Handle everyday research tasks with reliable, citation-backed results

Your personal Research Agent to handle research tasks with citation-backed results

Popular Tasks used by Researchers

How can I help with your research?

Meet SciSpace

Get more enhanced response by uploading the PDFs you want me to reference.

No relevant PDFs in your library

SciSpace is the AI research assistant for academics. Run systematic literature reviews on 280M+ papers, and write papers with cited sources. Trusted by 1M+ students, PhDs & researchers.

SciSpace | AI for Research

Analyze PDFs

Code & Manuscripts

Funding & Grants

Literature & Patents

Medical & Clinical Data

Systematic Review

Visualize & Present

Web & Data

Build a Google Scholar-like website for your research.

Build a website

Create charts and images for your research

Create a Chart

Write a paper for submission to a journal

Draft a manuscript

Patent Search

Design eye-catching scientific posters in minutes.

Scientific Poster Generation

Systematic Literature Review

One task is running at the moment. Your messages will be shown right after.

Drag and drop or click here to browse

Loved by <highlight>1 million+</highlight> researchers

Extract a list of specific topics and their sources from unstructured text

Topics

Compare and analyze relevant papers that matches with your search

Papers

Get insights from PDFs and bookmarked papers from your library

My library

Recent searches

Try searching for:

Catch AI-generated content in scholarly and non-scholarly content

{ai} Detector

Ai Writer

Get PDF Summaries, highlighted text explanations 

Chat with PDF

Effortlessly create in-text citations and bibliographies in APA and 2,500 other formats

Citation generator

Get explanations, summaries, and answers on academic papers

Ease up your research workflow with {scispace}'s cohort of exciting AI tools

Elevate your academic writing skills and convey your ideas the way you want

Paraphraser

Explore our range of reading and writing tools

Your file is being prepared and should be ready in a few minutes. If it's a large file, it might take a bit longer. You can close this window, and we'll email you the file when it's done.

You have reached a maximum limit of <strong>{limit}</strong> columns in the table. Remove at least <strong>1</strong> column to add or create another one.

C Brayne

Author Tools

Chat about Author