31,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Dominantly inherited Alzheimer's disease (DIAD) causes predictable biological changes decades before the onset of clinical symptoms, enabling testing of interventions in the asymptomatic and symptomatic stages to delay or slow disease progression. 2 key findings →
Evidence: high
Full summary, score breakdown and related studies → Original source
Identifying Aβ-positive individuals, irrespective of the measurement technique employed (CSF or PET), enables the detection of the most at-risk population before disease onset, or at least at a mild stage. 5 key findings →
Design: systematic review Participants: 7,793 Evidence: high
Full summary, score breakdown and related studies → Original source
The likelihood of amyloid positivity was associated with age and APOE ε4 status. 3 key findings →
Design: meta-analysis Participants: 377 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Phosphorylated tau (p-tau) species (153, 181, 217, 231) increased early in preclinical AD but were reduced with gantenerumab-mediated Aβ plaque reduction. 5 key findings →
Design: post-hoc analysis Participants: 50 Evidence: high
Full summary, score breakdown and related studies → Original source
Plasma Aβ40 values might not distinguish between PET (+) and PET (-) people. 2 key findings →
Design: meta-analysis Participants: 3,047 Evidence: high
Full summary, score breakdown and related studies → Original source
Concentrations of amyloid-beta (Aβ)(42) in the CSF appeared to decline 25 years before expected symptom onset. 5 key findings →
Design: cross-sectional Participants: 128 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
A total of 17 articles were identified. Plasma Aβ42/40 ratio was inversely correlated with aPET positivity r = -0.48 (95% confidence interval (CI): -0.65--0.31). 5 key findings →
Design: systematic review Participants: 17 Evidence: high
Full summary, score breakdown and related studies → Original source
In BioFINDER-2, the mean (SD) age was 65.7 (14.4) with 261 females (52.7%). 3 key findings →
Design: cohort Participants: 983 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Daily oral DHA supplementation (2 g/day) for 24 months may improve cognitive function and change blood biomarker-related Aβ-mediated autophagy in people with MCI. 2 key findings →
Participants: 120 Evidence: high
Full summary, score breakdown and related studies → Original source
Phosphorylated-tau (p-tau217) is a promising blood-based biomarker for Alzheimer's dementia (AD) in clinical settings. 3 key findings →
Design: cohort study Participants: 779 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Despite significant progress, applications of astrocyte biomarkers in AD remain in their early days. 4 key findings →
Design: systematic review Participants: 3,204 Evidence: high
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Alzheimer's disease neuropathology positivity was present in 86 (6%) participants based on p-tau217/Aβ42, 196 (15%) based on Aβ42/40, and 48 (4%) based on p-tau217, and was associated with worse performance on processing speed (standardised cognitive difference comparing Alzheimer's disease neuropathology positive to negative for Aβ42/40, p-tau217, and p-tau217/Aβ42 -0·54 to -0·25; p values 0·0001 to 0·0048) and executive function (-0·42 to -0·19; p values 0·0070 to 0·049). 3 key findings →
Design: cohort study Participants: 1,500 Evidence: moderate
Full summary, score breakdown and related studies → Original source
We demonstrated significant elevations in blood GFAP and YKL-40 levels in patients on the AD continuum compared with CU individuals. 5 key findings →
Design: systematic review Participants: 3,366 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Although APOE4 is strongly associated with amyloid-β (Aβ), its relationship with tau accumulation is less understood. 5 key findings →
Design: cross-sectional Participants: 1,370 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Neuroinflammation is a hallmark of Alzheimer's disease (AD) and both positive and negative associations of individual inflammation-related markers with brain structure and cognitive function have been described. 3 key findings →
Design: longitudinal study Participants: 295 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Study objectives To investigate the cumulative effect of five consecutive nights of partial sleep deprivation (PSD) on a panel of cerebrospinal fluid (CSF) biomarkers in healthy adults. 1 key finding →
Participants: 13 Evidence: high
Full summary, score breakdown and related studies → Original source
The distribution of tau pathology in Alzheimer's disease (AD) shows remarkable inter-individual heterogeneity, including hemispheric asymmetry. 1 key finding →
Design: longitudinal study Participants: 102 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Both plasma p-tau181 and GFAP appear to reflect disease progression, as indicated by 7T MR-derived brain changes which are not limited to areas known to be affected by tau pathology and neuroinflammation measured by MRS myo-inositol, respectively. 1 key finding →
Design: longitudinal study Participants: 127 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The main findings demonstrated an association between serum GFAP level and post-mortem tau pathology (β = 12.85; P < 0.001) that was independent of amyloid deposits (β = 13.23; P = 0.02). 5 key findings →
Design: cohort Participants: 139 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
These two conclusions support a dynamic biomarker model in which Alzheimer's disease is characterized first by the appearance of amyloidosis and later by tauopathy, with tauopathy being the proteinopathy associated with clinical symptoms. 1 key finding →
Design: longitudinal study Participants: 1,343 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Blood exosomes, which are extracellular vesicles secreted by living cells into the circulating blood, are regarded as a relatively noninvasive novel tool for monitoring brain physiology and disease states. 2 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source
Emerging plasma biomarkers of Alzheimer's disease might be non-invasive tools to trace early Alzheimer's disease-related abnormalities such as the accumulation of amyloid-beta peptides, neurofibrillary tau tangles, glial activation and neurodegeneration. 4 key findings →
Design: longitudinal study Participants: 164 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Modulating deposition of Aβ-containing plaques in the brain may be beneficial in treating Alzheimer's disease. β-site amyloid precursor protein cleaving enzyme 1 (BACE1) inhibitors have been shown to reduce Aβ in plasma and CSF in healthy volunteers. 1 key finding →
Evidence: high
Full summary, score breakdown and related studies → Original source
Among the individual plasma p-tau variants, p-tau217 consistently outperformed p-tau181 and p-tau231. 4 key findings →
Design: longitudinal study Participants: 352 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Cognition ranged from high to early cognitive decline (median Mini-Mental State Examination [MMSE] score = 26). 5 key findings →
Design: longitudinal study Participants: 60 Evidence: moderate
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 31,380 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 31,380 records, built mostly from automated pulls of Europe PMC (65.6% of the library) and OpenAlex (16.2%), 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.
1,048 records (3.3% of the library) are not peer-reviewed — 973 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 →
Newest studies, as a dated timeline → Atom feed Where this research is being discussed: events