27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
This includes adapting and disseminating care delivery innovations from one system to another, as well as measuring and sharing in the improved outcomes and reduced costs that might result. 5 key findings →
Design: systematic review Evidence: high
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It is estimated that for people aged 65 years and older, the risk of developing Alzheimer’s disease was nearly double for women compared with men (Weinstein et al., 2012). 5 key findings →
Evidence: low
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Alzheimer's disease (Alzheimer's), an ultimately fatal form of dementia, is the sixth leading cause of death in the United States, accounting for 3.6% of all deaths in 2014 (1,2). 3 key findings →
Participants: 93,541 Evidence: low
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The integration of artificial intelligence in medical image classification has significantly advanced disease detection. 2 key findings →
Evidence: low
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The “WarioWare: Move It!” intervention significantly improved physical flexibility, joint range of motion, motor coordination, hand dexterity, and cognitive function among older adults with mild cognitive impairment or dementia residing in rural LTCFs. 5 key findings →
Participants: 232 Evidence: low
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Despite elevated risk profiles for dementia, Black women are often absent in cultural narratives about dementia. 4 key findings →
Evidence: low
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Respondents who reported no difficulty deciding (DECIDE = 2) had substantially lower odds of SCD than those who reported difficulty (DECIDE = 1; aOR approximately 0.13; FDR < 0.05). 1 key finding →
Design: post-hoc analysis Participants: 298,944 Evidence: low
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BackgroundAsymptomatic carotid artery stenosis (ACAS) increases the risk of stroke, and is associated with cognitive decline. 5 key findings →
Design: systematic review Participants: 4,267 Evidence: high
Full summary, score breakdown and related studies → Original source
The term Precision Aging describes an approach that focuses on multi-domain profiles of risks impacting individual trajectories of age-related cognitive functioning. 3 key findings →
Participants: 555 Evidence: moderate
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Isolated REM sleep behaviour disorder (RBD) is the strongest prodromal marker of Parkinsons disease (PD) and dementia with Lewy bodies, yet diagnosis requires video-polysomnography with assisted montage and expert scoring and does not scale to screening or trial enrichment. 5 key findings →
Design: longitudinal study Participants: 378 Evidence: moderate
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INTRODUCTIONNovel capillary-blood collection methods have not yet been evaluated for a wide range of central nervous system (CNS) and neurodegenerative disease-related proteins. 2 key findings →
Evidence: low
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Alzheimers disease (AD) unfolds over decades preceding cognitive symptoms, and measuring the full scope of its molecular complexity remains difficult. 1 key finding →
Participants: 11,042 Evidence: low
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Parkinsons disease and dementia with Lewy bodies patients both demonstrated weaker global BOLD-CSF coupling compared to controls, with no detectable difference between patient groups. 4 key findings →
Participants: 39 Evidence: low
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The Dementia Trials Accelerator (DTA) is a UK-wide programme designed to improve the feasibility, efficiency, and inclusiveness of recruitment into clinical trials of dementia and related brain-health conditions. 5 key findings →
Participants: 10,000 Evidence: low
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Cognitively normal older adults are often regarded as a homogeneous population in preventive and disease-modifying clinical trials for dementia. 2 key findings →
Design: prospective cohort Participants: 1,136 Evidence: moderate
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BACKGROUNDQuantitative amyloid-beta (A{beta})-PET is increasingly used in AD prevention trials. 3 key findings →
Design: longitudinal study Participants: 433 Evidence: moderate
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BackgroundPathogenic variants in GCH1 have been associated with Parkinsons disease (PD), but the clinical phenotype and longitudinal disease course of GCH1-associated PD remain incompletely characterized. 5 key findings →
Design: longitudinal study Participants: 22,825 Evidence: moderate
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Cerebral small vessel disease (cSVD) is a leading cause of stroke and dementia. 5 key findings →
Evidence: low
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Cognitive and behavioural impairment frequently accompanies motor decline in amyotrophic lateral sclerosis (ALS), with 15% of cases meeting the diagnostic criteria for frontotemporal dementia (FTD). 2 key findings →
Evidence: low
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Structural variants (SVs) are a major source of genetic variation yet remain underexplored in healthy aging and neurodegenerative diseases. 1 key finding →
Evidence: low
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Genome-wide association studies (GWAS) typically represent Alzheimers disease (AD) risk loci by a single lead SNP, although the lead SNP may capture only part of the genetic variation at a locus. 3 key findings →
Participants: 493 Evidence: low
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Body mass index (BMI), type 2 diabetes (T2D) and related cardiometabolic features associate with Alzheimers disease (AD) risk, yet shared mechanisms remain poorly understood. 1 key finding →
Evidence: low
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Genetic variation at the TMEM106B locus has been associated with Alzheimers disease (AD) and related neurodegenerative phenotypes, yet its haplotypic architecture remains incompletely resolved. 2 key findings →
Participants: 493 Evidence: low
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BackgroundAlzheimers disease (AD) is characterized by amyloid beta and tau accumulation accompanied by altered inflammatory responses. 4 key findings →
Design: cross-sectional Participants: 261 Evidence: moderate
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Hexanucleotide repeat expansions in C9orf72 are the most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia, yet the predictive information contained within associated inflammatory and proteinopathy markers remains incompletely characterised. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Free full text links and the Full text may need a subscription label come from Unpaywall, Europe PMC and OpenAlex records of free copies, checked 10 Oct 2026. A study with neither is unknown, not paywalled. Show only studies that are free to read
This is alzhub's own score. It is not an official metric, not an impact factor, and no journal, publisher or ranking body endorses it. We built it so that a reader who is not a scientist can tell a landmark trial from a conference abstract without having to already know the difference. Every point comes from one of 20 components, all of them printed on the study itself, so you can disagree with our arithmetic rather than having to trust the total.
Journals are placed in ordered tiers, never given a numeric impact factor — we could not verify current impact factors from a source we control, and an invented one would be worse than none. Tier 1 is the top-tier general journals (NEJM, The Lancet, JAMA, Nature, Science, Nature Medicine); tier 2 is the leading specialty journals; tier 3 is every other peer-reviewed journal. A separate part scores how much the journal's own papers are cited, which tells the tier-3 journals apart.
Two rules we don't bend. First, we never fill in a missing value: if a record does not state a sample size or a design, that component scores zero, and if we simply have no data for a part, such as a citation count, that part is left out and the study is scored on the parts we could check. The study card says which. Second, anything that is not a peer-reviewed article is capped at 16/100 and carries a warning chip — so a conference abstract or a company press release can never outrank a peer-reviewed paper, no matter how good it looks.
We rank a rigorous null result — a good trial showing that something does not work — above an early positive finding. Someone deciding whether to buy a supplement is served by that, and the rigour is already counted by the design and journal components.
The score is computed from the published data alone and is reproducible: the same file always yields the same numbers.
See the whole rubric drawn out → — four charts covering all 27,380 studies: how the scores are spread and where the cap bites, which of the 20 components the library is strong and weak on, which subjects rest on stronger evidence, and what kinds of study each subject is actually built from.
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), plus smaller pulls from PubMed, Crossref and medRxiv. If a study, a drug, or a finding isn't here, that is not evidence it doesn't exist in the literature — it may simply not have been pulled in yet.
1,032 records (3.8% of the library) are not peer-reviewed — 962 of those are preprints posted before any journal review, and the rest are conference abstracts, regulatory notices and reports. Every study card on this page states its status plainly, and the score above is capped for anything that isn't a peer-reviewed article.
See the full, machine-readable breakdown of this library's coverage →