Preclinical studies indicate an age-associated accumulation of senescent cells across multiple organ systems. 3 key findings →
Design: open-label trial Evidence: high
Full summary, score breakdown and related studies → Original source
Research
31,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Gait speed for participants who worsened in CDR score during follow-up was slower at most examinations. 4 key findings →
Design: cohort study Participants: 287 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Lower CSF Aβ42, and higher t-tau/Aβ42 and p-tau/Aβ42 ratios were associated with BDI-II and BAI total scores, clinical depression (BDI-II ≥ 13), and clinical anxiety (BAI ≥ 10), as well as NPI-Q-assessed anxiety, apathy, and nighttime behavior. 3 key findings →
Design: cohort study Participants: 784 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The risk of mild cognitive impairment (MCI) or dementia in individuals with subjective cognitive decline (SCD) and biomarkers indicating Alzheimer disease (AD) pathology in comparison with individuals with SCD without biomarker evidence for AD is critical to delineate the potential role of biomarker assessment in this group. 4 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Alzheimer disease comorbid pathologic characteristics are common and are associated with more rapid cognitive decline in patients with dementia with Lewy bodies (DLB); therefore, it is anticipated that plasma p-tau concentrations may have utility in assessing cognitive impairment in individuals with this disorder. 4 key findings →
Design: cohort study Participants: 371 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Plasma phosphorylated tau at threonine 181 (p-tau181), a well-validated marker of Alzheimer disease (AD) pathologic change, could be a more efficient way to diagnose AD than invasive or expensive biomarkers requiring CSF or PET. 4 key findings →
Design: cross-sectional Participants: 571 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The temporal evolutions and relative orderings of Alzheimer disease biomarkers, including CSF amyloid-β42 (Aβ42), Aβ40, total tau (Tau) and phosphorylated tau181 (pTau181), standardized uptake value ratio (SUVR) from the molecular imaging of cerebral fibrillar amyloid-β with PET using the 11C-Pittsburgh Compound-B (PiB), MRI-based hippocampal volume and cortical thickness and cognition have been hypothesized but not yet fully tested with longitudinal data for all major biomarker modalities among cognitively normal individuals across the adult lifespan starting from 18 years. 4 key findings →
Design: longitudinal study Participants: 2,609 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
This study aimed to examine whether baseline CSF measures of Alzheimer disease (AD)-related pathology are associated with the time to onset of mild cognitive impairment (MCI) and whether these associations differ by age, sex, Apolipoprotein E ( ApoE4 ) status, and proximal (≤7 years) vs distal (>7 years) time to symptom onset. 4 key findings →
Design: longitudinal study Participants: 273 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Blood biomarkers indicative of Alzheimer's disease (AD) pathology are altered in both preclinical and symptomatic stages of the disease.
Full summary, score breakdown and related studies → Original source Free full text
Biomarkers were extracted from a total of 42 participants with longitudinal time points representing 164 imaging volumes. 5 key findings →
Design: longitudinal study Participants: 24 Evidence: moderate
Full summary, score breakdown and related studies → Original source
This study examined plasma phosphorylated tau 181 (P-tau181) and 217 (P-tau217) in 1,329 individuals aged 30-98 years from the population-based Mayo Clinic Study of Aging. 3 key findings →
Full summary, score breakdown and related studies → Original source Free full text
Sleep abnormalities are prevalent in Alzheimer's disease, with sleep quality already impaired at its preclinical stage. 4 key findings →
Design: cohort study Participants: 1,168 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
60/100
The neuropathologic changes underlying Alzheimer disease (AD) start before overt cognitive symptoms arise, but it is not well-known how they relate to the first subtle cognitive changes. 4 key findings →
Design: cross-sectional Participants: 217 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
There is an urgent need to improve the understanding of neuroinflammation in Alzheimer's disease (AD). 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
In this retrospective study, GAP-43 was measured in participants from the AD Neuroimaging Initiative (ADNI) cohort using an in-house ELISA method, and levels were compared between groups, both cross-sectionally and longitudinally. 4 key findings →
Participants: 786 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Heterozygosity of the KL-VS haplotype has been associated with reduced amyloid and tau burden. 4 key findings →
Design: case-control study Participants: 243 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Blood pressure variability is an emerging risk factor for cognitive decline and dementia, but mechanisms remain unclear. 4 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Two genetic variants in strong linkage disequilibrium (rs9536314 and rs9527025) in the Klotho (KL) gene, encoding a transmembrane protein, implicated in longevity and associated with brain resilience during normal aging, were recently shown to be associated with Alzheimer disease (AD) risk in cognitively normal participants who are APOE ε4 carriers. 4 key findings →
Participants: 5,541 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We compared digital speech and language features of patients with amnestic Alzheimer disease (aAD) or logopenic variant primary progressive aphasia (lvPPA) in a biologically confirmed cohort and related these features to neuropsychiatric test scores and CSF analytes. 4 key findings →
Design: cross-sectional Participants: 44 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Cerebrospinal fluid (CSF) tau and beta-amyloid levels in chronic traumatic encephalopathy (CTE), a disease which can be clinically indistinguishable from Alzheimer's disease (AD), are largely unknown. 4 key findings →
Design: cross-sectional Participants: 192 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
AUC-based performance was similarly good for the pTau181/Aβ42 ratio (AUC=0.841; 95% CI: 0.759-0.923), pTau181/Aβ40 ratio (AUC=0.837; 95% CI: 0.754-0.919), Aβ42/Aβ40 ratio (AUC=0.829; 95% CI: 0.746-0.912), tTau/Aβ42 ratio (AUC=0.822; 95% CI: 0.736-0.908), pTau181/Aβ42/Aβ40 ratio (AUC=0.817; 95% CI: 0.734-0.901), and Aβ42 (AUC=0.812; 95% CI: 0.722-0.902). 5 key findings →
Participants: 130 Evidence: low
Full summary, score breakdown and related studies → Original source
CSF biomarkers β-amyloid 1-42 (Aβ 42 ), phosphorylated tau 181 (p-tau 181 ), total tau (t-tau), and neurogranin (Ng) can diagnose Alzheimer disease (AD) in life. 4 key findings →
Participants: 61 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Previous studies reported the value of blood-based biomarkers in predicting Alzheimer disease (AD) progression among individuals with different disease stages. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
A total of 96 proteins were decreased in MCI-SNAP compared to CN and MCI-AD. 5 key findings →
Participants: 96 Evidence: low
Full summary, score breakdown and related studies → Original source
The apolipoprotein E (APOE)ε4 allele is the strongest genetic risk factor for late-onset AD and is associated with aberrant cerebrospinal fluid levels (CSF) of total tau (t-tau), phosphorylated tau (p-tau), and amyloid-β (Aβ). 4 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Where “Free full text” comes from
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
How the 0–100 score works — and why some entries are capped
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.
- Journal tier up to 10 pts
- Journal's citation record up to 4 pts
- Study design up to 12 pts
- Strength of evidence up to 5 pts
- Peer-review validation up to 10 pts
- How recent up to 5 pts
- Sample size up to 4 pts
- Effect reported up to 3 pts
- Studied in people up to 3 pts
- Randomized / blinded up to 2 pts
- Times cited up to 7 pts
- Citations per year up to 5 pts
- Impact for its field and year up to 6 pts
- Cited by studies here up to 6 pts
- Still being cited up to 4 pts
- Senior author's track record up to 4 pts
- Institution's track record up to 3 pts
- Multicenter collaboration up to 3 pts
- Indexed in PubMed up to 2 pts
- Free to read up to 2 pts
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.
What this library is — and isn't
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