CSF p-tau181 and p-tau231 biomarkers distinguished AD, MCI, and healthy populations. 2 key findings →
Participants: 5,017 Evidence: low
Full summary, score breakdown and related studies → Original source
Research
31,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
The systemic underrepresentation of Black participants in AD research impacts the ability to generalize research findings and determine the effectiveness and safety of disease-modifying treatments. 1 key finding →
Design: longitudinal study Participants: 629 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
This study suggests that the prognostic capacity of plasma NfL may be amplified in individuals with Aβ or hypertension. 5 key findings →
Design: longitudinal study Participants: 720 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
Hallucinations, delusions, and depression were more common in DLB than in AD and, in a subgroup with longitudinal follow-up, persistent hallucinations and NPSs were associated with lower p-tau181 and p-tau231 in DLB. 5 key findings →
Design: longitudinal study Participants: 222 Evidence: moderate
Full summary, score breakdown and related studies → Original source
None of the three plasma biomarker was associated with NPS at baseline. 5 key findings →
Design: longitudinal study Participants: 76 Evidence: moderate
Full summary, score breakdown and related studies → Original source
In general linear models lower plasma Aβ42/40 was related to lower visuospatial ability, higher total tau was related to lower episodic memory, and higher NfL was related to lower visuospatial ability and lower episodic memory. 3 key findings →
Design: cohort study Participants: 260 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Physical activity is a promising preventative strategy for Alzheimer's disease: it is associated with lower dementia risk, better cognition, greater brain volume and lower brain beta-amyloid. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
71/100
These findings indicate that plasma pTau181, plasma pTau217 and amyloid-β PET convey overlapping information and therefore predict the dynamic phase of asymptomatic amyloid-β accumulation with comparable performances. 1 key finding →
Design: cohort study Participants: 75 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Sleep is a potential early, modifiable risk factor for cognitive decline and dementia. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Aβ-PET was abnormal in 81 participants from J-TRC and 71 participants from BioFINDER. 2 key findings →
Design: cross-sectional Participants: 474 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Overall the study included 199 participants with iRBD, 20 hyposmic participants with available dopamine transporter single-photon emission computed tomography, 146 nonmanifest GBA1N409S gene carriers, 21 GBA1N409S gene carrier patients with PD, 50 patients with sporadic PD, and 140 healthy controls. 3 key findings →
Design: cross-sectional Participants: 170 Evidence: low
Full summary, score breakdown and related studies → Original source
Our review summarizes the diagnostic accuracy of plasma and cerebrospinal fluid (CSF) phosphorylated tau 217 (p-tau217) in detecting amyloid and tau pathology on positron emission tomography (PET). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
69/100
The mitochondrial cascade hypothesis of Alzheimer's disease (AD) has been portrayed through molecular, cellular, and animal studies; however large epidemiological studies are lacking. 3 key findings →
Design: cohort study Participants: 790 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Our findings suggest that plasma pTau181 is a promising biomarker for concurrent ADNC and amyloidosis in LBD. 3 key findings →
Design: longitudinal study Participants: 565 Evidence: moderate
Full summary, score breakdown and related studies → Original source
A total of 428 participants were included; 167 had normal cognition, 245 had MCI, and 16 had mild AD. 2 key findings →
Design: cross-sectional Participants: 428 Evidence: moderate
Full summary, score breakdown and related studies → Original source
These results suggested that distinct meta-cognitive profiles can be identified in preclinical-AD. 5 key findings →
Design: cohort study Participants: 314 Evidence: moderate
Full summary, score breakdown and related studies → Original source
In amyloid-negative cognitively unimpaired subjects, ApoE4 status influenced both baseline levels and rate of change of plasma p-tau217. 4 key findings →
Design: longitudinal study Participants: 151 Evidence: moderate
Full summary, score breakdown and related studies → Original source
69/100
After adjusting for retinal scan signal strength, neurofilament light chain showed a stronger negative association with retinal nerve fibre layer thickness [standardized beta estimate ( β ) = -0.184] and ganglion cell-inner plexiform layer thickness ( β = -0.139) compared to phosphorylated tau181, which exhibited weaker associations with ganglion cell-inner plexiform layer ( β = -0.091) and retinal nerve fibre layer ( β = -0.059). 3 key findings →
Design: cross-sectional Participants: 100 Evidence: low
Full summary, score breakdown and related studies → Original source
69/100
In TAP-TAU, we will investigate the added clinical value of tau-PET in a real-world clinical setting, including memory clinic patients with diagnostic uncertainty after routine work-up. 2 key findings →
Design: longitudinal study Participants: 300 Evidence: moderate
Full summary, score breakdown and related studies → Original source
This Swedish study of over 1,200 people with memory symptoms found that a blood test combining p-tau217 with an amyloid ratio (the 'Amyloid Probability Score 2') was far more accurate at identifying Alzheimer's disease than doctors' clinical judgment alone. 3 key findings →
Design: cross-sectional Participants: 1,213 Evidence: high
Full summary, score breakdown and related studies → Original source
Our study suggests a possible utility of plasma Aβ42/40, P-tau181, and P-tau231 as a noninvasive biomarkers to assess amyloid copathology in DLB, and plasma GFAP and NfL as monitoring biomarkers for cognitive symptoms in DLB. 4 key findings →
Design: cohort study Participants: 89 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
68/100
Baseline plasma VEGFA and PGF each showed a significant interaction with amyloid burden on prospective cognitive decline. 5 key findings →
Design: longitudinal study Participants: 317 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Brain volume analyses included 622 participants (mean age ± SD: 70.9 ± 10.2) with an average of 3.3 MRI scans over 4.7 years. 5 key findings →
Design: longitudinal study Participants: 622 Evidence: moderate
Full summary, score breakdown and related studies → Original source
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 31,780 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 31,780 records, built mostly from automated pulls of Europe PMC (66% of the library) and OpenAlex (16%), 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.
1,052 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