27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Regardless of method or adjustment, the resulting heritability estimates were highly variable across populations. 5 key findings →
Participants: 7,024 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Compared with men, women had greater amyloid burden (B = 0.05; 95% CI, 0.02-0.07; P < .001), Braak stages III and IV (B = 0.05; 95% CI, 0.02-0.08; P = .003) and Braak stages V and VI (B = 0.09; 95% CI, 0.06-0.12; P < .001) tau burden, and AD signature thickness (B = 0.04; 95% CI, 0.02-0.05; P < .001). 5 key findings →
Design: cross-sectional Participants: 501 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Four hundred eighty-six participants developed dementia during 37,782 person-years of follow-up. 5 key findings →
Participants: 5,205 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
γ-Secretase modulators (GSMs) represent an emerging oral therapy for preventing and targeting Aβ-amyloidosis in Alzheimer disease. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Cellular cross-talk, mediated by membrane receptors and their ligands, is crucial for brain homeostasis and can contribute to neurodegenerative diseases such as Alzheimer’s disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Current metabolomic aging clocks inadequately capture individual heterogeneity in biological aging trajectories, constraining their clinical utility. 4 key findings →
Participants: 196,790 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Cerebral small vessel disease (SVD) is frequently comorbid with Alzheimer's disease (AD), and brain endothelial cells (BECs) express genes associated with AD genetic risk. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD), the most common cause of dementia, is characterized by the accumulation of amyloid-β (Aβ) in senile plaques and abnormally hyperphosphorylated tau proteins in neurofibrillary tangles. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Mutations in the presenilin genes are the main cause of familial Alzheimer's disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Familial forms of frontotemporal dementia (FTD) with tauopathy are mostly caused by mutations in the gene encoding the microtubule-associated protein tau (MAPT). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Although multiple CHCHD10 mutations are associated with the spectrum of familial and sporadic frontotemporal dementia-amyotrophic lateral sclerosis (FTD-ALS) diseases, neither the normal function of endogenous CHCHD10 nor its role in the pathological milieu (that is, TDP-43 pathology) of FTD/ALS have been investigated. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Recently intronic and exonic mutations in the Tau gene have been found to be associated with familial neurodegenerative syndromes characterized not only by a predominantly frontotemporal dementia but also by the presence of neurological signs consistent with the dysfunction of multiple subcortical neuronal circuitries. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Epidemiological studies show that individuals who carry the relatively uncommon APOE ε2 allele rarely develop Alzheimer disease, and if they do, they have a later age of onset, milder clinical course, and less severe neuropathological findings than people without this allele. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Genetic mutations in the tau gene on chromosome 17 are known to cause frontotemporal dementias. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Detailed molecular pathology studies and clinicopathological phenotyping of familial amyotrophic lateral sclerosis (FALS) with characterised mutations in the gene encoding Cu/Zn superoxide dismutase (SOD1) will yield important insights into the pathogenesis of motor neuron degeneration. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Early life experience influences stress reactivity and mental health through effects on cognitive-emotional functions that are, in part, linked to gene expression in the dorsal and ventral hippocampus. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
These findings support evidence of genetic control of brain volume even in adults, particularly of hippocampal and neocortical volume and of cortical volumetric reductions being familial, but do not support measures of subcortical volumes per se as representing intermediate biologic phenotypes. 4 key findings →
Participants: 169 Evidence: low
Full summary, score breakdown and related studies → Original source
Major Depressive Disorder (MDD) is a common psychiatric disorder for which available medications are often not effective. 4 key findings →
Participants: 23 Evidence: low
Full summary, score breakdown and related studies → Original source
Familial Alzheimer's disease (fAD) mutations alter amyloid precursor protein (APP) cleavage by γ-secretase, increasing the proportion of longer amyloidogenic amyloid-β (Aβ) peptides. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid precursor protein (APP) mutations associated with familial Alzheimer's disease (AD) usually lead to increases in amyloid β-protein (Aβ) levels or aggregation. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
This case highlights potential long-term neurodegenerative outcomes in retired professional National Football League players subjected to repeated mild traumatic brain injury. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
APOE4 is the strongest genetic risk factor for Alzheimer's disease 1-3 . 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Health risk factors such as body mass index (BMI) and serum cholesterol are associated with many common diseases. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The human brain vasculature is of great medical importance: its dysfunction causes disability and death 1 , and the specialized structure it forms-the blood-brain barrier-impedes the treatment of nearly all brain disorders 2,3 . 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The identification of subjects at high risk for Alzheimer's disease is important for prognosis and early intervention. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
10 of the 3,521 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
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 →