In this large cohort of older adults, long-term PM2.5 exposure was associated with increased dementia incidence. 3 key findings →
Participants: 541 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Research
31,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
56 individuals (mean (sd) age: 68.8 (4.2) years, 26 females, 24/32 intervention/control group) were included at baseline and 41 returned after an average of 28 months for the second assessment. 5 key findings →
Design: randomized controlled trial Participants: 56 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
60/100
This Primer conceptualizes Alzheimer disease (AD) as a genetic and sporadic neurodegenerative disorder driven by a complex interplay between loss of synaptic homeostasis and endosomal/lysosomal clearance pathway dysfunction, in which Aβ and tau products play key roles. 4 key findings →
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
An estimated 40% of dementia is potentially preventable by modifying 12 risk factors throughout the life course. 4 key findings →
Participants: 39 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
During the past decade, a conceptual shift occurred in the field of Alzheimer's disease (AD) considering the disease as a continuum.
Full summary, score breakdown and related studies → Original source Free full text
This comprehensive analysis demonstrated that the variance in AD blood biomarker concentrations was mainly explained by age, with minor contributions from cognition, brain atrophy, and genetics, conversely to CSF measures. 3 key findings →
Participants: 2,323 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Copy-number variants (CNVs) are major contributors to human disease. 2 key findings →
Design: case-control Participants: 22,319 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Dementia diagnosis increasingly relies on blood-based biomarkers, yet their performance in diverse populations remains insufficiently characterized. 1 key finding →
Design: cross-sectional Participants: 605 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
57/100
Amyloid PET imaging has been crucial for detecting the accumulation of amyloid beta (Aβ) deposits in the brain and to study Alzheimer's disease (AD). 4 key findings →
Participants: 13,409 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Two of every three persons living with dementia reside in low- and middle-income countries (LMICs). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Dementia is an increasing focus for policymakers, civil organizations and multidisciplinary researchers. 5 key findings →
Design: narrative review Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Vitality was associated with disability primarily through the mediation of other IC domains. 2 key findings →
Design: longitudinal study Participants: 1,389 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
LIBRA might be a useful tool to identify individuals for primary prevention interventions of dementia in midlife, and maybe in late life, but not in the oldest-old. 2 key findings →
Participants: 3,256 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
'Covert' cerebral small vessel disease (ccSVD) is common on neuroimaging in persons without overt neurological manifestations, and increases the risk of future stroke, cognitive impairment, dependency, and death. 3 key findings →
Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Based on data from their first NACC visit with AD, there was considerable heterogeneity in language performance across people with EOAD and LOAD. 5 key findings →
Design: cross-sectional Participants: 1,189 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In vitro and animal studies have suggested that inoculation with herpes simplex virus 1 (HSV-1) can lead to amyloid deposits, hyperphosphorylation of tau, and/or neuronal loss. 4 key findings →
Participants: 58 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Cerebral small vessel disease (cSVD) is a leading cause of stroke and dementia with no specific treatment, of which molecular mechanisms remain poorly understood. 2 key findings →
Participants: 40,000 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We performed whole-exome and whole-genome sequencing in 927 late-onset Alzheimer disease (LOAD) cases, 852 early-onset AD (EOAD) cases, and 1273 controls from France. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
VLAHE residents had fewer hospitalizations and shorter stays (10.5 vs 15.2 days, P = .0004) than comparable NH residents, particularly for acute care. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Among the more than 90 identified genetic risk loci for late-onset Alzheimer's disease (AD) and related dementias, the apolipoprotein E (APOE) gene ɛ2/ɛ3/ɛ4 polymorphisms remain the longstanding benchmark for genetic disease risk with a consistently large effect across studies 1-10 . 5 key findings →
Design: case-control Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
The secreted peptide adropin is highly expressed in human brain tissues and correlates with RNA and proteomic risk indicators for dementia. 2 key findings →
Participants: 452 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Vision impairment is common among older adults and affects dementia screening assessments, which include visually presented items. 5 key findings →
Participants: 86 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Latin America’s diverse genetic landscape provides a unique opportunity to study Alzheimer’s disease (AD) and frontotemporal dementia (FTD). 1 key finding →
Participants: 2,162 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Multidomain interventions may benefit younger older adults or those with overly strict or lenient HbA1c control; however, these findings need confirmation in future studies. 3 key findings →
Participants: 531 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.
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 31,380 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 31,380 records, built mostly from automated pulls of Europe PMC (65.6% of the library) and OpenAlex (16.2%), 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.
1,048 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