27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Progressive neurodegenerative disorder i.e. Alzheimer’s disease (AD) is characterized by cognitive decline, oxidative stress, and cholinergic dysfunction, β-amyloid aggregation, tau hyperphosphorylation. 5 key findings →
Evidence: low
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The accumulation of tau proteins in the brain contributes to the therapeutic challenges faced by patients with Alzheimer’s disease, frontotemporal dementia, and other neurodegenerative disorders. 4 key findings →
Evidence: low
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The subscription based business model has significantly expanded beyond digital services, deeply penetrating the e-grocery and food delivery sectors. 3 key findings →
Evidence: low
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The results demonstrate similar poverty patterns as per county data findings on Kenya poverty report, 2022. 5 key findings →
Evidence: low
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Alzheimer’s disease (AD) pathology including amyloid beta (Aβ) plaques and tau tangles accumulate with age in Down Syndrome (DS). 4 key findings →
Evidence: low
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Individuals with Down syndrome (DS) display developmental delay, intellectual disability, premature brain ageing, and an increased risk of Alzheimer-like neurodegeneration. 4 key findings →
Evidence: low
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Alzheimer's disease progresses heterogeneously across diverse cohorts, yet current predictive models fail to capture this complexity while remaining clinically interpretable. 4 key findings →
Design: longitudinal study Participants: 1,669 Evidence: moderate
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There is high unmet need in dementia with Lewy bodies (DLB). 4 key findings →
Participants: 159 Evidence: high
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Blood biomarkers are increasingly used to support the diagnosis and monitoring of neurodegenerative diseases. 4 key findings →
Design: cross-sectional Participants: 5,123 Evidence: low
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These aggregated proteins contribute to the pathological and clinical heterogeneity of AD and are associated with a more rapid progression. 4 key findings →
Participants: 1,304 Evidence: low
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Increasing evidence suggests that accurate prediction of Alzheimer’s disease (AD) symptom onset requires more than amyloid- and tau-centric biomarkers such as cerebrospinal fluid (CSF) Aβ42/40, total tau and p-tau181 and plasma p-tau217. 4 key findings →
Participants: 484 Evidence: low
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In neurodegenerative diseases, the diagnostic value of α-synuclein seed amplification assay (αSAA) in routine clinical practice and its relationship with cognitive performance and fluid biomarkers remains incompletely characterized. 4 key findings →
Participants: 398 Evidence: moderate
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We investigated whether vascular and lifestyle factors are associated with AD plasma and imaging biomarkers in midlife. 4 key findings →
Participants: 1,406 Evidence: low
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Blood-based biomarkers could transform Alzheimer disease (AD) detection by enabling scalable, less invasive assessment of underlying pathology, yet their applicability across globally diverse populations remains uncertain. 4 key findings →
Design: meta-analysis Evidence: high
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Alzheimer disease (AD) pathology begins 15–20 years before clinical symptoms, necessitating non - invasive biomarkers for early diagnosis. 4 key findings →
Participants: 120 Evidence: low
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We estimated associations of educational attainment and Alzheimer disease genetic risk with treatment initiation and incident dementia and compared GLP-1 receptor agonist initiators with initiators of non-sodium-glucose cotransporter 2 inhibitor second-line therapies, with a separate sodium-glucose cotransporter 2 inhibitor compa 4 key findings →
Design: cohort study Participants: 14,364 Evidence: moderate
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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
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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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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 →