27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
& objective Evidence is limited on how estimated glomerular filtration rate (eGFR) and urinary albumin-creatinine ratio (UACR) relate to dementia at different ages. 4 key findings →
Design: cohort study Participants: 9,967 Evidence: moderate
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This study examines whether neuroticism is differentially associated with risk of incident Alzheimer's disease (AD), vascular dementia (VD), and frontotemporal dementia (FTD) using a prospective study design. 4 key findings →
Participants: 401,422 Evidence: low
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Current dementia risk scores have had limited success in consistently identifying at-risk individuals across different ages and geographical locations. 4 key findings →
Participants: 176 Evidence: moderate
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Whether or not there is targeted pharmacotherapy for dementia, an active and healthy lifestyle that includes physical activity (PA) may be a better option than medication for preventing dementia. 4 key findings →
Participants: 484,169 Evidence: low
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Neurodegenerative diseases are characterised by neuronal loss and cerebral deposition of proteins with altered physicochemical properties. 4 key findings →
Participants: 233 Evidence: low
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Relating clinical symptoms to neuroanatomical profiles of brain damage and ultimately to tissue pathology is a key challenge in the field of neurodegenerative disease and particularly relevant to the heterogeneous disorders that comprise the frontotemporal lobar degeneration spectrum. 4 key findings →
Evidence: moderate
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We recently surveyed the relationship between the human brain transcriptome and genome in a series of neuropathologically normal postmortem samples. 4 key findings →
Participants: 188 Evidence: moderate
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No treatment for frontotemporal dementia (FTD), the second most common type of early-onset dementia, is available, but therapeutics are being investigated to target the 2 main proteins associated with FTD pathological subtypes: TDP-43 (FTLD-TDP) and tau (FTLD-tau). 4 key findings →
Evidence: moderate
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Magnetic resonance (MR) imaging is used widely for assessment of patients with cognitive impairment, but the pathological correlates are unclear, especially when multiple pathologies are present. 4 key findings →
Participants: 93 Evidence: moderate
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Although previous research has shown that initiation of postmenopausal estrogen hormone therapy (HT) in late life increases risk of dementia, animal studies and some observational studies have suggested that midlife use of HT may be beneficial; however, this has not been rigorously investigated in large population-based studies. 4 key findings →
Participants: 1,524 Evidence: low
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Patients with Alzheimer's disease have reduced cerebral blood flow measured by arterial spin labelling magnetic resonance imaging, but it is unclear how this is related to amyloid-β pathology. 4 key findings →
Participants: 51 Evidence: low
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The amyloid hypothesis for Alzheimer's disease (AD) posits a neuron-centric, linear cascade initiated by Aβ and leading to dementia. 3 key findings →
Evidence: low
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Alterations in α-synuclein dosage lead to familial Parkinson's disease (PD), and its accumulation results in synucleinopathies that include PD, dementia with Lewy bodies (DLB) and multiple system atrophy (MSA). 4 key findings →
Evidence: low
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Of 285 297 total patients, 180 283 (63.2%) were female; 586 (0.2%) were American Indian/Alaska Native, 8957 (3.1%) Asian, 28 694 (10.1%) Black, 7406 (2.6%) Hispanic, 1959 (0.7%) Native Hawaiian/Pacific Islander, 237 017 (83.1%) non-Hispanic White, and 678 (0.2%) multiracial individuals. 5 key findings →
Design: cross-sectional Participants: 178 Evidence: low
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In cognitively unimpaired (CU) adults at baseline, the risk for progression to dementia increased for every decile increase in the ADI state ranking (hazard ratio = 1.06, 95% confidence interval (1.01-1.11), P = .01). 5 key findings →
Participants: 4,699 Evidence: low
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Among 9239 eligible respondents, 5258 (57.7%) were female and 1210 (9.1%) were Black, 574 (4.7%) were Hispanic, and 7297 (84.4%) were White. 5 key findings →
Design: cohort study Evidence: moderate
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(n = 2,392) had a mean age of 74.4 years, 60.4% were female, and 17.1% were of self-reported Black race. 5 key findings →
Design: cross-sectional Participants: 2,392 Evidence: low
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On average, participants were aged 63 years and had 16 years of education. 5 key findings →
Design: randomized controlled trial Participants: 100 Evidence: high
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All ML models outperformed the MMSE alone. 5 key findings →
Design: longitudinal study Participants: 1,331 Evidence: moderate
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Cross-ancestry sex-stratified analyses identified several loci with evidence of interaction (p 0.05). 5 key findings →
Design: meta-analysis Participants: 25,284 Evidence: high
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The study encompassed 479 723 participants (mean [SD] age, 56.5 [8.1] years; 260 730 females [54.4%]), including 271 690 in the YOD analyses and 334 939 in the LOD analyses. 5 key findings →
Design: cohort study Participants: 723 Evidence: moderate
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DSD is linked to adverse outcomes, compared to dementia alone, like longer hospitalisation [3], mortality [3, 4], functional decline [3] and need for residential care [3]. 4 key findings →
Design: systematic review Participants: 64 Evidence: high
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Among the 1665 AIBL participants (741 [44.5%] female) and 2029 ADNI participants (925 [45.6%] female), the mean (SD) age at first evaluation was 71.8 (7.1) years and 74.5 (6.7) years, respectively. 5 key findings →
Design: cohort study Evidence: moderate
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Here we show that the associations of 57 metabolites with dementia risk varied by APOE4 genotype or other AD/ADRD risk variants. 3 key findings →
Evidence: low
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The introduction of incretin mimetics (IMs), including glucagon-like peptide-1 receptor agonists (GLP-1 RAs) such as liraglutide and semaglutide, as well as dual GLP-1/glucose-dependent insulinotropic polypeptide receptor co-agonists (GLP-1/GIP RAs) like tirzepatide, has revolutionized obesity treatment. 2 key findings →
Design: meta-analysis Evidence: high
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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.
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 →