PD patients who develop poor outcomes show lower DTI-ALPS, potentially reflecting impaired glymphatic clearance. 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Research
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
In this sample, the high-throughput blood Aβ assay was not able to distinguish well between AD patients and controls. 2 key findings →
Design: case-control study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Although genetic Aβ variants cause early-onset Alzheimer's disease, literature reports on Aβ properties are heterogeneous, obscuring molecular mechanisms, as illustrated by recent failures of Aβ-level targeting trials. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Our findings indicate differential relationships between comorbidities (demographic, medical, diagnostic) across NHB, Hispanic, and NHW participants. 5 key findings →
Participants: 764 Evidence: moderate
Full summary, score breakdown and related studies → Original source
It is an open issue whether blood biomarkers serve to diagnose Alzheimer's disease (AD) or monitor its progression over time from prodromal stages. 2 key findings →
Design: longitudinal study Participants: 76 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Our findings demonstrate that distinct inflammatory molecules are associated with different cognitive disorders. 5 key findings →
Participants: 131 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Hippocampal subfields with distinctive atrophy patterns may mediate the effects of tau pathology on cognitive function. 2 key findings →
Design: cross-sectional Participants: 40 Evidence: low
Full summary, score breakdown and related studies → Original source
60/100
Circulating metabolites can identify biochemical risk factors related to Alzheimer's disease (AD). 3 key findings →
Participants: 1,068 Evidence: low
Full summary, score breakdown and related studies → Original source
ACAD's traction indicates the feasibility of recruiting Asians for clinical research to enhance understanding of AD risk factors. 1 key finding →
Participants: 606 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a neurodegenerative disease characterised by neuropathological hallmarks, including extracellular amyloid plaques and neurofibrillary tangles. 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Highlights Mild behavioral impairment (MBI) is linked to elevated plasma p-tau217, a specific Alzheimer's disease biomarker.MBI increases the odds of plasma p-tau217 positivity in dementia-free individuals. 1 key finding →
Participants: 101 Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma p-tau217 concentrations, considered together with APOE genotype, might help stratify risk and estimate the timing of future cognitive impairment in asymptomatic individuals who are at increased risk for Alzheimer's disease, such as those with a family history of dementia or known APOE-ε4 carrier status. 5 key findings →
Design: cohort Participants: 8,582 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Ascertainment of the -synuclein level in CSF somewhat improves the differential diagnosis of AD vs DLB and PDD when combined with established AD biomarkers. 3 key findings →
Design: cross-sectional Participants: 453 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
These optimized thresholds can help to inform future research and clinical trials targeting early Aβ. 2 key findings →
Participants: 342 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Cerebrospinal fluid (CSF) biomarkers are useful in the diagnosis and the prediction of progression of several neurodegenerative diseases. 2 key findings →
Participants: 535 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Plasma NfL level is a valuable noninvasive biomarker that supplements magnetic resonance imaging scans and possibly reflects the severity of CSVD burden. 3 key findings →
Design: cross-sectional Participants: 496 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Performance was assessed in comparison to clinical diagnosis (blinded to plasma results) and amyloid status (CSF/PET). 4 key findings →
Participants: 268 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
AD was common in both AD-related syndromes (110/125 [88%]) and FTLD-related syndromes (45/198 [23%]). 2 key findings →
Participants: 125 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The quality of included studies with only a few longitudinal studies, limits the conclusions which may be drawn from the present findings especially regarding the biomarkers other than hippocampal volume. 4 key findings →
Design: systematic review Participants: 40 Evidence: high
Full summary, score breakdown and related studies → Original source Full text may need a subscription
The pTau217/Aβ42 ratio demonstrated the highest diagnostic accuracy, with an AUC of 0.927 (0.900-0.954). 3 key findings →
Participants: 423 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
These findings suggest an association of sHHV infection with white matter volume loss, attentional decline, and astrogliosis. 5 key findings →
Design: cross-sectional Participants: 119 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
CSF Aβ 42 and PiB PET showed maximal correlation when collected within 6 years of each other ( R ≈ -0.5). 1 key finding →
Design: longitudinal study Participants: 371 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Higher baseline p-tau181 and NfL were associated with significantly faster decline in most cognitive, physical, and functional outcomes (+1 SD p-tau181: β MMSE = -0.055, 95% CI -0.067 to -0.043, β FCSRT = -0.034, 95% CI -0.043 to -0.025, β fluency = -0.029, 95% CI -0.038 to -0.020, β SPPB = -0.040, 95% CI -0.057 to -0.022, and β 4IADL = -0.115, 95% CI 0.091-0.140. +1 SD NfL: β MMSE = -0.039, 95% CI -0.053 to -0.025, β FCSRT = -0.022, 95% CI -0.032 to -0.012, β fluency = -0.014, 95% CI -0.024 to -0.004, and β 4IADL = 0.077, 95% CI 0.048-0.105). 4 key findings →
Participants: 1,938 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Among the 12 biomarkers, only pTau was higher in frail individuals than in their not-frail peers (471.3 ± 58.1 pg/mL vs. 451.9 ± 61.1 pg/mL, p = 0.022). 4 key findings →
Design: longitudinal study Participants: 313 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Plasma β-synuclein demonstrated discriminative properties for Aβ PET positive and negative subjects. 3 key findings →
Design: longitudinal study Participants: 51 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
- Randomised / 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
- Multi-centre 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 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.
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 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 →