27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Plasma tau partly reflects AD pathology, but the overlap between normal aging and AD is large, especially in patients without dementia. 3 key findings →
Design: longitudinal study Participants: 179 Evidence: moderate
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At 6 months, galantamine significantly improved cognition and global function. 2 key findings →
Design: open-label trial Participants: 636 Evidence: low
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Patients' mean age was 73.6 years (range 48 to 92 years). 2 key findings →
Participants: 144 Evidence: high
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Although conclusions are limited by small sample size and the possibility of a type II error, results suggest that short-term estrogen therapy does not improve symptoms of most women with AD. 5 key findings →
Evidence: high
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MCR is common in older adults, and is a strong and early risk factor for cognitive decline. 3 key findings →
Design: cohort study Participants: 26,802 Evidence: moderate
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We tested the hypothesis that plasma neurofilament light chain (NfL) identifies asymptomatic carriers of familial frontotemporal lobar degeneration (FTLD)-causing mutations at risk of disease progression. 4 key findings →
Design: longitudinal study Participants: 277 Evidence: moderate
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Midlife p-tau181 was associated with faster 11-year memory decline beginning 20 years later in the ARIC cohort, which underscores a potentially long prodromal phase of cognitive decline that could precede dementia onset. 5 key findings →
Design: prospective cohort Participants: 920 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Conjugated equine estrogens with or without MPA are associated with greater brain atrophy among women aged 65 years and older; however, the adverse effects are most evident in women experiencing cognitive deficits before initiating hormone therapy. 3 key findings →
Evidence: high
Full summary, score breakdown and related studies → Original source
Our data show that elderly patients with DM without dementia have accelerated progression of brain atrophy with significant consequences in cognition compared to subjects without DM. 5 key findings →
Design: randomized controlled trial Participants: 89 Evidence: high
Full summary, score breakdown and related studies → Original source
A long-term CMI in ChEI-treated early Alzheimer disease patients produced additional mood and cognitive benefits. 1 key finding →
Evidence: high
Full summary, score breakdown and related studies → Original source
The beneficial effect of DBS on motor function was stable and comparable by target over 36 months. 3 key findings →
Design: randomized controlled trial Participants: 89 Evidence: high
Full summary, score breakdown and related studies → Original source
This randomized trial of 406 spouse caregivers of people with Alzheimer's tested whether counseling and support (six counseling sessions, mandatory support groups, and on-call phone counseling) could delay nursing home placement. 3 key findings →
Design: RCT Participants: 406 Evidence: high
Full summary, score breakdown and related studies → Original source
In moderate stages of amnestic mild cognitive impairment, common cognitive tests provide better predictive accuracy than measures of whole brain, ventricular, entorhinal cortex, or hippocampal volumes for assessing progression to Alzheimer disease. 1 key finding →
Participants: 129 Evidence: high
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Greater access to effective programs of counseling and support could yield considerable benefits for caregivers, patients with Alzheimer disease, and society. 2 key findings →
Design: randomized controlled trial Evidence: high
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We included randomized controlled trials (RCTs) and nonrandomized controlled studies at lower risk of bias comparing ChEI treatment with placebo or usual treatment, for 6 months or longer, in patients with dementia of any type. 5 key findings →
Design: systematic review Participants: 79,153 Evidence: high
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The majority of community-dwelling older persons have brain pathology. 2 key findings →
Design: cohort study Participants: 80 Evidence: moderate
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Neuroinflammation and cerebrovascular dysfunction are early events occurring already at presymptomatic stages of AD and contribute to disease progression. 5 key findings →
Design: longitudinal study Participants: 508 Evidence: moderate
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Central obesity in midlife increases risk of dementia independent of diabetes and cardiovascular comorbidities. 3 key findings →
Design: longitudinal study Participants: 1,049 Evidence: moderate
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We carried out a double-blind study of a vasopressin-related peptide, DGAVP citrate (Org 5667), in 115 patients with mild dementia, probable Alzheimer's type (DAT). 2 key findings →
Participants: 115 Evidence: low
Full summary, score breakdown and related studies → Original source
A total of 408 participants were included (n = 221 were LATE-NC+/HS-, n = 145 were LATE-NC+/HS+, and n = 42 were LATE-NC-/HS+). 5 key findings →
Design: cohort study Participants: 221 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The best CSF measures for identifying MCI-AD were Aβ42/total tau (t-tau) and Aβ42/hyperphosphorylated tau (p-tau) (area under the curve [AUC] 0.93-0.94). 3 key findings →
Design: longitudinal study Participants: 122 Evidence: moderate
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In response to sleep loss (+17.2%), compared with normal sleep (+1.8%), the evening to morning ratio was increased for t-tau ( p = 0.035). 4 key findings →
Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
In participants with early symptomatic AD, zagotenemab failed to achieve significant slowing of clinical disease progression compared with placebo. 5 key findings →
Design: clinical trial Participants: 360 Evidence: high
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We demonstrated significant elevations in blood GFAP and YKL-40 levels in patients on the AD continuum compared with CU individuals. 5 key findings →
Design: systematic review Participants: 3,366 Evidence: high
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Patients with MCI converted to AD at an annual rate of 17.2%. 2 key findings →
Design: longitudinal study Participants: 85 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
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
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.
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.
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 →