For both cohorts, the prevalence of mosaicism was 40 and Aβ 42 concentrations. 2 key findings →
Design: longitudinal study Participants: 357 Evidence: moderate
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.
From a total sample of 559 older adults from the Massachusetts Alzheimer's Disease Research Center longitudinal cohort, 454 were included in the primary analysis: 283 with clinically normal cognition (CN), 115 with mild cognitive impairment (MCI), and 56 with subjective cognitive concerns (SCC) but no objective impairment, a proposed transitional group between CN and MCI. 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Short-term memory dysfunction is a key early feature of Alzheimer's disease (AD). 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Positive cerebrospinal fluid (CSF) biomarkers of tau and amyloid beta42 suggest possible active underlying Alzheimer's disease (AD) including neurometabolic dysfunction and neurodegeneration leading to eventual cognitive decline. 4 key findings →
Design: cohort study Participants: 82 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The sensitivity of amyloid to pre-analytic factors complicates cerebrospinal fluid (CSF) diagnostics for Alzheimer disease. 4 key findings →
Design: longitudinal study Participants: 727 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
A possible involvement of the gene IL1RAP (interleukin-1 receptor-associated protein) in the pathogenesis of Alzheimer's disease (AD) has been suggested in GWASs of cerebrospinal fluid (CSF) tau levels and longitudinal change in brain amyloid burden. 4 key findings →
Design: longitudinal study Participants: 3,446 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
It remains unknown whether the associations between protective lifestyles and sporadic dementia risk reported in observational studies also affect age at symptom onset (AAO) in autosomal dominant Alzheimer disease (ADAD) with predominant genetic influences. 4 key findings →
Design: longitudinal study Participants: 103 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The patient was participating in an extended open-label trial of aducanumab when she was admitted to hospital for focal seizures and ARIA in 2 noncontiguous regions of the left frontal and occipital lobes. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
135 subjects enrolled in a longitudinal clinicopathologic study were administered the MoCA by a single physician and the MMSE by a trained research assistant. 4 key findings →
Design: longitudinal study Participants: 135 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
59 recruiting sites for the Alzheimer's Disease Neuroimaging Initiative. 4 key findings →
Design: cohort study Participants: 41 Evidence: moderate
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Alzheimer's disease (AD), the most common type of dementia, is a severe neurodegenerative disorder. 4 key findings →
Design: longitudinal study Evidence: moderate
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There is evidence that major depression increases the risk for dementia, but there is conflicting evidence as to whether depression may accelerate cognitive decline in dementia. 4 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The CDR® plus NACC FTLD was able to detect early symptoms in the mildly impaired participants who were rated as CDR® sum of boxes (CDR®-SB) = 0. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Even before dementia becomes apparent, cognitive decline may contribute to deterioration in oral health. 4 key findings →
Design: cohort study Participants: 10,050 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The study formed part of the Rotterdam Study, a prospective, population-based cohort study on the frequency, etiology, and prognosis of chronic diseases. 4 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
We studied compliance with antihypertensive treatment in elderly patients with cognitive impairment. 4 key findings →
Design: cohort study Participants: 1,979 Evidence: moderate
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Mental symptoms have been shown to be associated with dementia. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
A lack of understanding of the causes of attrition in longitudinal studies of older adults may lead to higher attrition rates and bias longitudinal study results. 4 key findings →
Design: longitudinal study Participants: 30,433 Evidence: moderate
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At autopsy the striatal dopaminergic transporter is reduced. 4 key findings →
Design: cohort study Evidence: moderate
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Totally 7499 participants were included in the analysis, representing 40,728,543 community-living older Americans. 5 key findings →
Design: longitudinal study Participants: 7,499 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Individuals with rapid progression were more likely to have at least one APOE ε4 allele (OR: 2.08 [95% CI: 1.16–3.74], p < 0.01), higher Braak stage (2.19 [1.20–3.98], p < 0.01), higher Thal phase (2.45 [1.24–4.83], p < 0.01), more severe white matter rarefaction (1.68 [1.21–2.35], p < 0.01), and in the final 24 months of life, more frequent untreated/undertreated hyperlipidemia (1.74 [1.35–5.56], p < 0.01) and less frequent untreated/undertreated depression (0.40 [0.17–0.91], p < 0.05). 3 key findings →
Design: cohort study Participants: 75 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
ARIA-positive patients had significantly higher Fazekas scores compared with ARIA-negative patients (1.37 versus 1.0; P = .0262), indicating a greater DWMH burden. 5 key findings →
Design: cohort study Participants: 27 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
This cohort study compares the risk of incident all-cause dementia among people with hearing loss who use vs do not use hearing aids. 1 key finding →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Approximately half (54.5%, 35/55) of participants showed a decline in RBMT scores during the 2-year follow-up and were defined as the memory decline group. 4 key findings →
Design: longitudinal study Participants: 55 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
During follow-up ranging from 1.0 to 22.9 years, 75 patients (29.88%) converted to AD. 5 key findings →
Design: longitudinal study Participants: 75 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 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 →