28,980 Alzheimer's and dementia studies in plain English, each scored out of 100.
Self-report of poor sleep was associated with greater AD-related pathology in cognitively healthy adults at risk for AD. 3 key findings →
Participants: 101 Evidence: moderate
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Pericyte damage, reflected by CSF PDGFRβ, may be involved in age-related BBB disruption together with neuroinflammation, but is not related to Alzheimer-related pathologic changes. 2 key findings →
Participants: 408 Evidence: moderate
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Aβ deposition increases slowly from cognitive normality to moderate severity DAT. 5 key findings →
Participants: 206 Evidence: low
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Median (interquartile range) CRP levels increased with mean (SD) age (43.3 [9.6] years, 0.95 mg/L [0.40-2.35 mg/L] vs 59.1 [9.6] years, 2.04 mg/L [0.93-4.75 mg/L] vs 61.6 [9.5] years, 2.21 mg/L [1.05-5.12 mg/L]; P Conclusions and relevance In this study, peripheral chronic low-grade inflammation in participants with ApoE4 was associated with shortened latency for onset of AD. 2 key findings →
Design: cohort study Evidence: moderate
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Naproxen may attenuate cognitive decline in slow decliners while accelerating decline in fast decliners. 2 key findings →
Participants: 2,388 Evidence: low
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In a large IRBD cohort diagnosed in a tertiary referal sleep center, prolonged follow-up indicated that the majority of patients are eventually diagnosed with the synucleinopathies PD, DLB and less frequently MSA. 3 key findings →
Participants: 174 Evidence: moderate
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We tested the hypotheses that TDP-43 with Alzheimer's disease pathology is a common mixed pathology; is related to increased likelihood of expressing clinical Alzheimer's-type dementia; and that TDP-43 pathologic stage is an important determinant of clinical Alzheimer's-type dementia. 5 key findings →
Participants: 398 Evidence: moderate
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Neuropathological and in vivo studies have revealed a tight relationship between tau pathology and cognitive impairment across the Alzheimer's disease spectrum. 5 key findings →
Participants: 40 Evidence: low
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Limited evidence suggests that the APOEε4 allele may confer risk for CTE, but previous studies were small with limited scope. 5 key findings →
Design: cross-sectional Participants: 294 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Complexity at multiple levels needs to be understood and overcome to develop effective treatments and preventions for cognitive decline and AD dementia. 1 key finding →
Design: cohort study Evidence: moderate
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A consensus panel from the United States and Europe was convened recently to update and revise the 1997 consensus guidelines for the neuropathologic evaluation of Alzheimer's disease (AD) and other diseases of brain that are common in the elderly. 2 key findings →
Evidence: low
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The spread of protein aggregates during disease progression is a common theme underlying many neurodegenerative diseases. 3 key findings →
Evidence: low
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Synaptic dysfunction occurs early in senile dementias, presumably as a result of decreased levels of functional synaptic proteins as found in autopsied brains of patients with Alzheimer's disease (AD) or frontotemporal dementia (FTD). 3 key findings →
Design: cross-sectional Participants: 12 Evidence: moderate
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We used a new method of pooling cerebrospinal fluid Aβ42 and Pittsburgh compound B positron emission tomography measures to produce equivalent measures of brain Aβ load from either source and analysed the results using multiple imputation methods. 3 key findings →
Participants: 165 Evidence: low
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To characterize antibodies produced in humans in response to Abeta42 vaccination, we carried out immunohistochemical examinations of the brains of both transgenic mice and human patients with beta-amyloid pathology. 4 key findings →
Evidence: low
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Microglia play a pivotal role in the maintenance of brain homeostasis but lose homeostatic function during neurodegenerative disorders. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Debate surrounds the role of chronic pain as a risk factor for cognitive decline and dementia. 4 key findings →
Design: longitudinal study Participants: 995 Evidence: moderate
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We postulated that cerebral amyloid angiopathy (CAA), characterised by cortical vascular amyloid deposits, is associated with cortical tissue loss independent of parenchymal Alzheimer's disease pathology. 4 key findings →
Design: case-control study Participants: 63 Evidence: moderate
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To better understand clinical and neuropathological features of TDP-43 proteinopathies, data were analyzed from autopsied research volunteers who were followed in the National Alzheimer's Coordinating Center (NACC) data set. 4 key findings →
Design: longitudinal study Participants: 495 Evidence: moderate
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We have undertaken a large unselected, community-based neuropathology study in an elderly (70-103 years) UK population in relation to prospectively evaluated dementia status. 4 key findings →
Participants: 209 Evidence: low
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Amyotrophic lateral sclerosis (ALS) is a common, fatal motor neuron disorder with no effective treatment. 4 key findings →
Participants: 111 Evidence: low
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The neuropathologic substrate of amnestic mild cognitive impairment (aMCI) is not known. 4 key findings →
Design: cohort study Participants: 23 Evidence: moderate
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The degree to which Alzheimer's versus other neuropathologies contribute to the risk of Alzheimer's dementia is unknown. 4 key findings →
Participants: 1,161 Evidence: low
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Although it is clear that astrocytes and microglia cluster around dense-core amyloid plaques in Alzheimer disease (AD), whether they are primarily attracted to amyloid deposits or are just reacting to plaque-associated neuritic damage remains elusive. 4 key findings →
Evidence: low
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In a total of 602 autopsy cases (median [IQR] age at death, 78 [71-85] years; 328 male [54.5%] and 274 female [45.5%]), higher PM2.5 exposure prior to death was associated with increased odds of more severe Alzheimer disease neuropathologic change (ADNC) (odds ratio, 1.19; 95% CI, 1.11-1.28). 5 key findings →
Design: cohort study Participants: 602 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
10 of the 7,799 studies in this tag that have a study page, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
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 28,980 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 28,980 records, built mostly from automated pulls of Europe PMC (62.8% of the library) and OpenAlex (17.6%), 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.
1,038 records (3.6% of the library) are not peer-reviewed — 966 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 →