43/100
= 18 556) lived in care homes before death. 4 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Research
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
The statistical analysis revealed that the survival time was significantly longer in females compared to males (p = 0.003). 5 key findings →
Design: cohort study Participants: 54 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
hexanucleotide repeat expansions (HRE) and WMH in bvFTD patients. bvFTD and svPPA are associated with elevated WMH burden independent of CVRF. 3 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
MCI exhibited greater retinal tortuosity (p < 0.05) and sparser vasculature (p < 0.001), correlating with higher PSMD, WMH volumes, and adverse plasma biomarkers (all p < 0.05). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Genetic variants increase the risk of neurocognitive disorders in later life, including vascular dementia (VaD) and Alzheimer’s disease (AD), but the precise relationships between genetic risk factors and underlying disease etiologies are not well understood. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Amyloid status moderated associations between IIV-dispersion and WMH, such that higher IIV-dispersion was associated with greater WMH in Aß+ individuals whether WMH was examined as a continuous (B = 0.30, ß = 0.13, p = .006) or a dichotomous variable based on quartiles (odds ratio [OR] = 2.41, p < .001). 4 key findings →
Participants: 819 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
), whereas the effect of region was only borderline-significant when comparing NAWM, WML peripheries and WML (p = 0.03) and non-significant for the other comparisons (p > 0.29). 3 key findings →
Participants: 56 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
= 0.71) longitudinally. YKL-40 associations with FW and FW-corrected fractional anisotropy were null. 4 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Each 1-SD increase in eGDR was significantly associated with a reduction in WMH volume (β = -0.057; 95% CI: -0.062 to -0.051; p 0.05). 3 key findings →
Participants: 34,789 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Lower DTI-ALPS, lower BOLD-CSF coupling, and higher CP volume predicted dementia, but PVS volume did not. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Of the 130,605 included patients with ischemic stroke, 12,696 (9.7%) patients developed SHS. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The results of the inverse variance weighted analysis demonstrate a significant positive causal relationship between stroke and VaD (OR = 2.06, 95% confidence interval [CI] = 1.17-3.61, P = .01). 5 key findings →
Participants: 222 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Vascular contributions to cognitive impairment and dementia (VCID) represent a major public health challenge in the aging population, with age-related cerebromicrovascular dysfunction playing a critical role in its development. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Older stroke survivors engaging in regular PA had a 38 % reduced risk of dementia [Odds Ratio (OR) =0.62, 95 % Confidence Interval (CI): 0.56-0.69, P < 0.001] and a 44 % lower risk of mortality [Hazard Ratio (HR) =0.56, 95 % CI: 0.52-0.59, P < 0.001]. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
43/100
Alzheimer's disease, the leading cause of dementia, is a multifactorial disorder involving amyloid beta (Aβ) and tau deposition, impaired glucose metabolism, neuroinflammation, mitochondrial dysfunction, insulin resistance, and progressive brain atrophy. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Reimbursement decisions for new Alzheimer's disease (AD) treatments are informed by economic evaluations. 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Neighborhood deprivation is associated with shorter survival, cognitive impairment and neurodegeneration in aging and Alzheimer's disease. 3 key findings →
Design: longitudinal study Participants: 161 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The sense of food insecurity in a group of elderly people may be determined by the perception of distance to food outlets. 1 key finding →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Whilst nursing home managers recognise the potential benefits of advance care planning, barriers and challenges create a reluctance to facilitate. 3 key findings →
Participants: 178 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
These results suggest that both current physical activity and levels of amyloid can be important predictors of spatial navigation skills. 5 key findings →
Design: longitudinal study Participants: 65 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Mild cognitive impairment in Parkinson's disease research has progressed from basic mechanism exploration to a multidisciplinary, integrated clinical-basic stage, following an evolutionary path of "pathological mechanism - clinical phenotype - biomarker - intervention strategy." 2 key findings →
Design: systematic review Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
There is increasing use of neuroimaging modalities, including PET, for diagnosing dementia. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Human genetic and animal model studies indicate that brain microglial inflammation is a primary driver of cognitive impairment in Alzheimer Disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The concentration of 124 I-RmAb158-scFv8D3, as measured in vivo with PET, increased with age and corresponded well with the ex vivo autoradiography and Aβ immunohistochemistry results. 5 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The hTau40(AT) mice mimic pathological hallmarks of tauopathies including a cognitive phenotype combined with pronounced neuroinflammation visible by bioluminescence. 2 key findings →
Evidence: low
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.
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 27,380 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 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), 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.
1,032 records (3.8% 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 →