28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Social isolation was associated with elevated blood-based biomarkers of neuronal injury, with variation by patterns of exposure over time. 5 key findings →
Participants: 3,862 Evidence: low
Full summary, score breakdown and related studies → Original source
Test-retest reliability measures are essential for interpretation of meaningful effects over time for plasma and digital outcomes. 1 key finding →
Participants: 92 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Chronic Wasting Disease (CWD) is a fatal transmissible spongiform encephalopathy (TSE) that is confined to cervids (deer, moose, elk, and reindeer) but shares key properties with human neurodegenerative conditions such as Alzheimer’s, Parkinson’s, Huntington’s disease and frontal-temporal dementia. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Bidirectional stepwise linear regression analysis was performed to identify plasma biomarkers associated with brain Aβ deposition. 5 key findings →
Design: cohort study Participants: 541 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The observed phenotypic and genetic associations highlight shared underlying mechanisms among plasma biomarkers. 2 key findings →
Participants: 696 Evidence: low
Full summary, score breakdown and related studies → Original source
a Structured abstract BACKGROUND Over the past couple of decades, the role of infections, as well as the involvement of the immune system, have been highlighted in the development of dementia. 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
The clock claims are unsupported. 3 key findings →
Design: longitudinal study Participants: 83 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease primarily affecting motor neurons but also frequently involving cognitive impairment. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
The full cohort included 1044 participants, of whom 779 comprised the proteomics cohort. 5 key findings →
Design: longitudinal study Participants: 674 Evidence: moderate
Full summary, score breakdown and related studies → Original source
These findings support MRI-derived LC intensity as a marker of early AD-related processes and suggest that LC intensity may provide complementary information not captured by plasma pTau 217 alone. 4 key findings →
Design: longitudinal study Participants: 163 Evidence: moderate
Full summary, score breakdown and related studies → Original source
A prespecified structure–reserve–glial profile captured reproducible cognitive variation beyond measured Alzheimer disease molecular pathology across two cohorts. 1 key finding →
Design: longitudinal study Participants: 436 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Complement-mediated neuroinflammation has been implicated in Alzheimer’s disease (AD), but its role during the pre-symptomatic phase of the disease remains unclear. 4 key findings →
Participants: 708 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Amyloid regional extent and tau PET were associated with different features of dyadic CFI data: reporter balance and CFI burden across reporters, respectively. 4 key findings →
Design: cross-sectional Participants: 1,686 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease pathology and cognitive outcomes frequently diverge, yet current single-axis definitions cannot identify resilient (high pathology, preserved cognition) and resistant (high risk, low pathology) subgroups reliably at scale, obscuring the mechanisms that uncouple pathological burden from cognitive decline. 2 key findings →
Participants: 1,009 Evidence: moderate
Full summary, score breakdown and related studies → Original source
CSF Aβ42 rose from 526.0 to 1053.0 pg/mL (+ 100.2%), total tau (t-tau) fell from 578.2 to 278.0 pg/mL(-51.9%), and phosphorylated tau181 (p-tau181) fell from 90.8 to 23.1 pg/mL(-74.6%). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Electrochemical biosensors offer a promising route for the rapid, non-invasive detection of disease biomarkers by converting biochemical interactions into measurable electrical signals. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma pTau-181 demonstrates flat or declining longitudinal trajectories and minimal cognitive correlation, suggesting tau is a static biomarker rather than a dynamic therapeutic target in mid-to-late adulthood. 2 key findings →
Design: cross-sectional Participants: 2,523 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Our findings confirm the diagnostic value of urinary β-amyloid protein detection in MCI and AD-related dementia. 5 key findings →
Design: case-control study Participants: 51,187 Evidence: high
Full summary, score breakdown and related studies → Original source
Among 2711 decedents (mean [SD] age, 73.4 [14.4] years; range, 23 to 111 years; 1340 [49.4%] female), 531 (19.6%) met both thresholds, 270 (10.0%) the amyloid threshold only, 207 (7.6%) the tau threshold only, and 1703 (62.8%) neither. 3 key findings →
Design: cross-sectional Participants: 1,467 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Most plasma proteomic studies in Alzheimer’s disease (AD) compare cases and controls cross-sectionally, leaving unresolved which AD-associated proteins mark diagnostic states and which are linked to disease progression. 5 key findings →
Design: longitudinal study Participants: 13,449 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Dementia with Lewy bodies (DLB) is a common neurodegenerative dementia that remains difficult to distinguish clinically from Alzheimer's disease (AD) and related disorders because of overlapping clinical features and frequent mixed pathology. 4 key findings →
Participants: 20 Evidence: low
Full summary, score breakdown and related studies → Original source
Scalable and accessible biomarkers of neurofibrillary tangle pathology are needed for Alzheimer’s disease prognosis, diagnosis and monitoring. 4 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
In a contemporary, diverse cohort, most established dementia risk algorithms had limited power in discriminating amyloid positivity, pTau-217 positivity, and current cognitive status despite acceptable calibration. 3 key findings →
Participants: 603 Evidence: moderate
Full summary, score breakdown and related studies → Original source
We validated results in CSF from 397 participants in the Accelerated Medicine Partnership-Alzheimer’s Disease cohort. 5 key findings →
Participants: 500 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Our findings suggest that serum brain-derived p-tau 217 and SV2A are more specific diagnostic biomarkers for reflecting brain damage and may not be disturbed by peripheral damage for AD patients. 5 key findings →
Design: cross-sectional Participants: 1,198 Evidence: moderate
Full summary, score breakdown and related studies → Original source
10 of the 727 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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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 (3.7% 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 →