OSA may aggravate cognitive dysfunction in dementia and thus may be a reversible cause of cognitive loss in patients with AD. 3 key findings →
Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Research
27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Studies were significantly heterogeneous in terms of country, outcomes assessed, and the timing of post-ED outcome assessments. 5 key findings →
Design: systematic review Participants: 7,940 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Elevated blood pressure during midlife, persistence of elevated blood pressure into late life, and, among nonhypertensives, a steep decline in blood pressure during mid- to late life were associated with an increased dementia risk in a community-based cohort. 5 key findings →
Participants: 1,440 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Down syndrome (DS) is a genetic form of Alzheimer's disease (AD) that offers crucial insights into AD pathogenesis. 2 key findings →
Design: cohort study Participants: 1,135 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Accumulating evidence demonstrates that metabolic changes in the brain associated with neuroinflammation, oxidative stress, and mitochondrial dysfunction play an important role in the pathophysiology of mild cognitive impairment (MCI) and Alzheimer's disease (AD). 4 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
However, few longitudinal Pittsburgh compound B-positron emission tomography studies have tested this hypothesis, and with conflicting results. 5 key findings →
Design: longitudinal study Participants: 32 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Previous conclusions of a lack of efficacy for cognitive training in MCI may have been influenced by not clearly defining the intervention. 1 key finding →
Design: systematic review Participants: 305 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
In persons selected from a population-based study, elevated amyloid levels at baseline were associated with worse cognition and imaging biomarkers at baseline and with greater clinical decline and neurodegeneration. 5 key findings →
Design: longitudinal study Participants: 286 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
This kMCT drink improved cognitive outcomes in MCI, at least in part by increasing blood ketone level. 1 key finding →
Participants: 39 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
67/100
This study provides evidence for sex differences in the progression to cognitive impairment in PD, while specific cognitive features become more important indicators of progression with impending conversion to PDD. 3 key findings →
Design: longitudinal study Participants: 418 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The SCIENCe study confirms that SCD is a heterogeneous group, with preclinical AD and subthreshold psychiatric features. 4 key findings →
Design: cohort study Participants: 114 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
67/100
The APOE-ε4 allele is associated with a moderately increased risk for progression from MCI to AD-type dementia. 4 key findings →
Design: meta-analysis Participants: 35 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Cox proportional hazards regression, adjusted for age at baseline, gender, apolipoprotein genotype, and NYU paragraph delayed recall score, showed that higher BDI scores were associated with progression to AD (p = 0.03). 4 key findings →
Participants: 208 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
A diagnosis of COPD is associated with an increased risk for MCI, particularly NA-MCI. 5 key findings →
Design: cross-sectional Participants: 1,425 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
See Li and Donohue (doi:10.1093/brain/awy089) for a scientific commentary on this article. 4 key findings →
Design: longitudinal study Participants: 338 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
TREM2 encodes for triggering receptor expressed on myeloid cells 2 and has rare, coding variants that associate with risk for late-onset Alzheimer's disease (LOAD) in Caucasians of European and North-American origin. 4 key findings →
Design: case-control study Participants: 800 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
A rare coding variant (rs72824905, p.P522R) conferring protection against Alzheimer's disease (AD) was identified in the gene encoding the enzyme phospholipase-C-γ2 (PLCG2) that is highly expressed in microglia. 4 key findings →
Design: longitudinal study Participants: 10,097 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
67/100
A rare TREM2 missense mutation (rs75932628-T) was reported to confer a significant Alzheimer's disease (AD) risk. 4 key findings →
Design: meta-analysis Participants: 89,157 Evidence: high
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Blood biomarkers able to diagnose Alzheimer disease (AD) at the preclinical stage would enable trial enrollment when the disease is potentially reversible. 4 key findings →
Design: case-control study Participants: 161 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
This study included patients with clinical SCD and SCD-free, healthy control (HC) participants with available baseline CSF and/or longitudinal cognitive data from the observational DZNE Longitudinal Cognitive Impairment and Dementia study. 4 key findings →
Design: longitudinal study Participants: 672 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Understanding the neuropathological effects of amyloid β (Aβ)-targeting therapies and amyloid-related imaging abnormalities (ARIA) in Alzheimer's disease is critical for optimising treatment efficacy and patient outcomes. 4 key findings →
Design: case-control study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Five databases were searched for English-language studies up to August 2010, and included all study designs with a comparative group. 4 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
67/100
Florbetapir F 18 PET can image amyloid-β (Aβ) aggregates in the brains of living subjects. 4 key findings →
Design: longitudinal study Participants: 51 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
In a recent crossover trial, methylphenidate treatment decreased apathy in Alzheimer's disease. 4 key findings →
Participants: 37 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
This study aimed to investigate the association between a virtual reality (VR) intervention program and cognitive, brain and physical functions in high-risk older adults. 4 key findings →
Design: randomized controlled trial Participants: 68 Evidence: high
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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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 →