27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Based on this meta-analytic survey of the literature, increased amyloid burden has small but nontrivial associations with specific domains of cognitive performance in individuals who are currently cognitively normal. 3 key findings →
Design: meta-analysis Participants: 7,140 Evidence: high
Full summary, score breakdown and related studies → Original source
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
Full summary, score breakdown and related studies → Original source Free full text
APOE ε4 may influence the association between WMH and cognitive performance in AD and DLB. 5 key findings →
Design: meta-analysis Participants: 167 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Our prospective findings provide evidence for what may be an early contributory role of systemic inflammation in neurodegeneration and cognitive aging. 3 key findings →
Design: cohort study Participants: 1,633 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Our findings suggest that tau PET is more sensitive than Aβ PET and measures of cortical thickness for detecting early cognitive changes in preclinical AD. 2 key findings →
Design: cross-sectional Participants: 106 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Thinning in specific cortical areas known to be affected by Alzheimer disease (AD) is detectable in individuals with questionable AD dementia (QAD) and predicts conversion to mild AD dementia. 3 key findings →
Design: longitudinal study Participants: 49 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Longitudinal studies will be required to determine the association of elevated [(11)C]PIB binding and risk of developing dementia of the Alzheimer type. 2 key findings →
Design: longitudinal study Evidence: moderate
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Hippocampal volume was the primary determinant of memory decline, whereas executive function (EXEC) decline was related to multiple brain components. 5 key findings →
Design: longitudinal study Participants: 103 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
In this longitudinal study of cognitively unimpaired adults, living in the most highly disadvantaged neighborhoods was associated with accelerated degeneration in Alzheimer signature regions and cognitive decline. 5 key findings →
Design: longitudinal study Participants: 19 Evidence: moderate
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In clinically normal older adults, lower functional connectivity predicted more rapid decline in PACC scores over time, particularly when coupled with increased Aβ burden. 2 key findings →
Design: longitudinal study Participants: 237 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
During the period of longitudinal observation, which averaged 32.6 months, 27 of the 80 MCI patients became demented. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
GOF indices were highest in normal controls, intermediate in MCI, and lowest in AD (p Conclusions fMRI connectivity indices distinguish patients with MCI who undergo cognitive decline and conversion to AD from those who remain stable over a 2- to 3-year follow-up period. 3 key findings →
Design: cross-sectional Participants: 68 Evidence: moderate
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Atrophy is not uniform across regions, nor does it follow a linear trajectory. 2 key findings →
Design: longitudinal study Participants: 472 Evidence: moderate
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In an older cohort with low cerebrovascular disease burden, T2DM contributes to cognitive decline via neurodegeneration. 3 key findings →
Design: longitudinal study Participants: 124 Evidence: moderate
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In this in vivo study, we have demonstrated that microglial activation quantified using [ 11 C]PBR28 PET was associated with higher gray matter volume and higher hippocampal volume in patients with MCI. 4 key findings →
Design: longitudinal study Participants: 55 Evidence: moderate
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These results suggest that WMH primarily affect the risk of progression when CSF measures of neurodegeneration or neuronal injury (as reflected by t-tau) are low. 5 key findings →
Design: longitudinal study Participants: 274 Evidence: moderate
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Rates of hippocampal atrophy (%/year) were 0.0 +/- 0.8 in the absent, 1.7 +/- 0.4 in the moderate, and 3.6 +/- 1.0 in the severe (mean +/- SD) tertile. 2 key findings →
Participants: 323 Evidence: moderate
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Hippocampal and entorhinal cortex volumes were each largest in controls, intermediate in MCI nonconverters, and smallest in MCI converters to AD (37 of 139 patients converted to AD). 1 key finding →
Participants: 139 Evidence: low
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Abnormal levels of all biomarkers were associated with faster time to cognitive impairment, and some participants with abnormal biomarker levels remained cognitively normal for up to 6.6 years. 2 key findings →
Design: longitudinal study Participants: 201 Evidence: moderate
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Brain atrophy with aging was observed in supratentorial and infratentorial areas, as well in primary motor, sensory, and heteromodal association regions. 1 key finding →
Design: longitudinal study Participants: 33 Evidence: moderate
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Increased amygdalar diffusivity in the absence of tissue loss in dementia with Lewy bodies (DLB) may be related to microvacuolation, a common pathology associated with Lewy body disease in the amygdala. 3 key findings →
Design: case-control study Participants: 30 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Acceleration in WMH burden, a common indicator of cerebrovascular disease in the elderly, is a pathologic change that emerges early in the presymptomatic phase leading to MCI. 2 key findings →
Design: longitudinal study Participants: 134 Evidence: moderate
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Carriers (n = 39) and noncarriers (n = 36) had similar neuropsychological performance, except for lower Letter Digit Substitution Test scores in carriers. 5 key findings →
Design: case-control study Participants: 39 Evidence: moderate
Full summary, score breakdown and related studies → Original source
These findings suggest a potential vasculoprotective role of vitamin D. 2 key findings →
Design: cross-sectional Participants: 318 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Aging-associated WMHs evolve significantly over a 4-year period. 5 key findings →
Design: longitudinal study Participants: 150 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 →