28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
Olfactory identification deficit is a useful screening tool for AD-related amnestic disorder, with sensitivity and specificity comparable to other established biomarkers, with benefits such as ease of administration and low cost. 1 key finding →
Design: cross-sectional Participants: 96 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Deposition of amyloid-β (Aβ) in the brain parenchyma and vessels is one of the hallmarks of Alzheimer disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The C9orf72 expansion is a common cause of ALS and FTLD, but not of AD or PD. 4 key findings →
Participants: 520 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Hypometabolism in PiB-positive, cognitively normal subjects in a population-based cohort occurs in AD-signature cortical regions and to a lesser extent in other cortical regions. 4 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Apolipoprotein E (apoE) alleles determine the age-adjusted relative risk (epsilon4 > epsilon3) for Alzheimer's disease (AD).
Full summary, score breakdown and related studies → Original source Free full text
The major known genetic risk for Alzheimer's disease (AD), apolipoprotein E-4 (APOE-4), is associated with lowered parietal, temporal, and posterior cingulate cerebral glucose metabolism in patients with a clinical diagnosis of AD. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
We identified a PSEN1 (presenilin 1) mutation carrier from the world's largest autosomal dominant Alzheimer's disease kindred, who did not develop mild cognitive impairment until her seventies, three decades after the expected age of clinical onset. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
By multiple logistic regression, the APOE-epsilon 4 allele frequency was significantly higher in the patients positive for HSV1 in brain than in the HSV1-negative AD group, the HSV1-positive non-AD group, or the HSV1-negative non-AD group (52.8% vs 10.0%, 3.6%, and 6.3%, respectively). 3 key findings →
Participants: 40 Evidence: low
Full summary, score breakdown and related studies → Original source
Corticobasal degeneration (CBD) is a neurodegenerative tauopathy-a class of disorders in which the tau protein forms insoluble inclusions in the brain-that is characterized by motor and cognitive disturbances 1-3 . 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Causes of the well-documented association between low levels of cognitive functioning and many adverse neuropsychiatric outcomes, poorer physical health and earlier death remain unknown. 4 key findings →
Participants: 112 Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a complex disorder influenced by environmental and genetic factors. 1 key finding →
Participants: 10,922 Evidence: low
Full summary, score breakdown and related studies → Original source
We used a collection of 708 prospectively collected autopsied brains to assess the methylation state of the brain's DNA in relation to Alzheimer's disease (AD). 2 key findings →
Participants: 117 Evidence: low
Full summary, score breakdown and related studies → Original source
The role of DNA cytosine methylation, an epigenetic regulator of chromatin structure and function, during normal and pathological brain development and aging remains unclear. 1 key finding →
Participants: 125 Evidence: moderate
Full summary, score breakdown and related studies → Original source
An 8-plex version of an isobaric reagent for the quantitation of proteins using shotgun methods is presented. 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
We investigated associations between apolipoprotein E (APOE) alleles and motor manifestations in Alzheimer's dementia (AD) capitalizing on National Alzheimer's Coordinating Center data: the baseline evaluations of older adults (≥60 years) with a diagnosis of AD were analyzed. 3 key findings →
Participants: 389 Evidence: low
Full summary, score breakdown and related studies → Original source
A total of 37 SuperAgers (73% female, mean [standard deviation] 82.7 [2.8] years old) and 35 controls (54% female, 83.7 [4.3] years old) were included. 5 key findings →
Participants: 37 Evidence: low
Full summary, score breakdown and related studies → Original source
Hippocampal subfield atrophy is a prime structural change in the brain, associated with cognitive aging and neurodegenerative diseases such as Alzheimer's disease. 3 key findings →
Participants: 1,086 Evidence: low
Full summary, score breakdown and related studies → Original source
Clinical genetic diagnosis was achieved in 7 of 50 (14%) of the patients, with a further 8 patients (16%) found to have established risk factors which may have contributed to their EOD. 5 key findings →
Participants: 50 Evidence: moderate
Full summary, score breakdown and related studies → Original source
A total of 1,350 publications with 59,818 citations were identified. 5 key findings →
Participants: 1,350 Evidence: low
Full summary, score breakdown and related studies → Original source
We performed a genome-wide association study (GWAS) of human extreme longevity (EL), defined as surviving past the 99th survival percentile, by aggregating data from four centenarian studies. 4 key findings →
Participants: 2,304 Evidence: low
Full summary, score breakdown and related studies → Original source
OptPRS predicted AD dementia and Aβ positivity, independent of apolipoprotein E (APOE). 5 key findings →
Participants: 1,634 Evidence: low
Full summary, score breakdown and related studies → Original source
Two ABCA7 missense variants (rs3764647 and rs3752239) demonstrated significant association with AD risk. 4 key findings →
Participants: 319 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Thirteen pathway clusters were identified, and eight pathway-specific PRSs were significantly associated with AD diagnosis. 5 key findings →
Participants: 1,411 Evidence: low
Full summary, score breakdown and related studies → Original source
The pathogenic relevance in Alzheimer's disease (AD) presents a decrease of cerebrospinal fluid amyloid-ß42 (Aß42) burden and an increase in cerebrospinal fluid total tau (T-tau) levels. 3 key findings →
Participants: 843 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Using the data from the Alzheimer's Disease Neuroimaging Initiative (ADNI), we performed a genome-wide association study (GWAS) between 565,373 single nucleotide polymorphisms (SNPs) and 16 key AD biomarkers from 1,576 subjects at four visits. 5 key findings →
Participants: 1,576 Evidence: low
Full summary, score breakdown and related studies → Original source
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 28,580 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 28,580 records, built mostly from automated pulls of Europe PMC (62.2% of the library) and OpenAlex (17.8%), 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.
1,034 records (3.6% 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 →