Accumulating white matter changes in advanced age are likely driven by small-vessel ischemic disease. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
30,980 Alzheimer's and dementia studies in plain English, each scored out of 100.
Accumulating white matter changes in advanced age are likely driven by small-vessel ischemic disease. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
CA1 apical neuropil atrophy is apparent in patients with mild AD. 2 key findings →
Design: cross-sectional Participants: 14 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
These findings suggest that DMN fcMRI may prove useful as a biomarker across a wide spectrum of disease, and support the feasibility of DMN fcMRI as a secondary endpoint in upcoming multicenter clinical trials in Alzheimer disease. 2 key findings →
Design: cross-sectional Evidence: moderate
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MeDi groups were comparable for clinical and neuropsychological measures. 2 key findings →
Participants: 34 Evidence: low
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Plasma A beta levels are affected by age and by systemic and CNS vascular risk factors. 4 key findings →
Design: cross-sectional Participants: 55 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Previous studies reported substantial contributions of neurofibrillary tangles (NFT), amyloid deposits, and neuronal loss to the development of dementia. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We investigated the associations between retinopathy and dementia and its subtypes Alzheimer disease (AD) and vascular dementia both cross-sectionally and prospectively in the Rotterdam Study, a large population-based cohort study. 4 key findings →
Design: cohort study Participants: 195 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The discovery cohort contained 3,671 individuals with a mean age of 68 years and consisted of 49% reported female. 5 key findings →
Participants: 3,671 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
= 0.009). Other neuropathologies were similar across cognitive groups. 4 key findings →
Design: cohort study Participants: 40 Evidence: moderate
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The incidence of amyloid PET positivity is approximately 13% per year among CN participants over age 70 sampled from a population-based cohort. 4 key findings →
Participants: 207 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Our findings suggest that the informant report is particularly relevant in patients with MCI where it strongly relates to higher amyloid-PET, indicative of impairment due to AD. 2 key findings →
Design: cross-sectional Participants: 25 Evidence: moderate
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Even in a highly selected lifespan sample of adults, Aβ deposition is apparent in some adults and is influenced by APOE status. 5 key findings →
Participants: 137 Evidence: low
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Mean IGF-1 levels were 144 ± 60 μg/L in generation 1 and 114 ± 37 μg/L in generation 2. 3 key findings →
Participants: 789 Evidence: low
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As potential harbingers of future cognitive decline, physicians should query and monitor SMCs from their older patients. 1 key finding →
Participants: 531 Evidence: moderate
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Lowering brain Aβ must be accomplished early in the evolution of AD. 4 key findings →
Participants: 475 Evidence: low
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In recent years, accumulating evidence has suggested that vascular risk factors contribute to Alzheimer disease (AD). 1 key finding →
Evidence: low
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The late-life dementia risk index accurately stratified older adults into those with low, moderate, and high risk of developing dementia. 2 key findings →
Participants: 480 Evidence: low
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Magnetic resonance imaging (MRI)-based volumetric measurements of medial temporal lobe (MTL) structures can discriminate between normal elderly control subjects and patients with Alzheimer's disease (AD) of moderate to advanced severity. 1 key finding →
Participants: 94 Evidence: low
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Hippocampal atrophy is not specific for AD but is also seen in semantic dementia. 2 key findings →
Participants: 26 Evidence: low
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The frontal lobes are most severely affected by SIVD. 4 key findings →
Participants: 78 Evidence: low
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During follow-up, 13 healthy patients converted to MCI or Alzheimer disease (AD), whereas 39 MCI subjects converted to AD. 5 key findings →
Participants: 72 Evidence: low
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Subjective cognitive failures (SCF) are associated with lower hippocampal volume, even in subjects without objective cognitive impairment and independent of white matter lesions. 2 key findings →
Design: cohort study Participants: 503 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Global cortical amyloid burden is high in dementia with Lewy bodies (DLB) but low in Parkinson disease dementia. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
A staging system based on this conceptual model of cerebrovascular pathology could enable the neuropathologic quantification of the cerebrovascular burden in dementia. 2 key findings →
Participants: 26 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Among elderly Medicare beneficiaries with PD, race, sex, and neighborhood SES are strong independent predictors of DBS receipt. 5 key findings →
Design: cohort study 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.
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 30,980 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 30,980 records, built mostly from automated pulls of Europe PMC (65.2% of the library) and OpenAlex (16.4%), 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.
1,042 records (3.4% of the library) are not peer-reviewed — 967 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