28,980 Alzheimer's and dementia studies in plain English, each scored out of 100.
Frontotemporal lobar degeneration, the neuropathological substrate of frontotemporal dementia (FTD), is characterized by the deposition of protein aggregates, including tau. 4 key findings →
Participants: 99 Evidence: low
Full summary, score breakdown and related studies → Original source
OptPRS predicted AD dementia and Aβ positivity, independent of apolipoprotein E (APOE). 5 key findings →
Participants: 1,634 Evidence: low
Full summary, score breakdown and related studies → Original source
Dysregulation of sphingomyelin and ceramide metabolism have been implicated in Alzheimer's disease. 1 key finding →
Participants: 1,576 Evidence: low
Full summary, score breakdown and related studies → Original source
Subjects without amyloid, including three with pathologically confirmed corticobasal degeneration, showed greater regional 18F-AV-1451 retention and associated regional atrophy in areas commonly associated with corticobasal degeneration pathology than healthy control subjects [retention was higher compared to healthy controls (P = 0.0011), driven especially by the precentral gyrus (P = 0.011) and pallidum (P < 0.0001), and greater atrophy was seen in subjects compared to control subjects (P = 0.0004)]. 3 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
CAA-PRS was significantly associated with pathological CAA (OR = 1.766, p < 0.001), with an AUC of 0.783 overall and 0.766 (OR = 1.780, p = 0.002) in those with high amyloid burden. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) and hearing loss (HL) are major age-related public health challenges with emerging evidence suggesting their interconnection. 2 key findings →
Participants: 349 Evidence: low
Full summary, score breakdown and related studies → Original source
A total of 124 participants with Alzheimer disease, cerebrovascular disease, or a mix Alzheimer's and cerebrovascular diseases and 55 controlparticipants underwent magnetic resonance imaging and neuropsychological testing. 5 key findings →
Participants: 124 Evidence: low
Full summary, score breakdown and related studies → Original source
We found that AD cases with comorbid LATE-NC, AD(LATE-NC+), have increased burdens of pretangles and/or NFTs as well as increased brain levels of p-tau199, compared to AD(LATE-NC-) cases and controls. 5 key findings →
Participants: 98 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Concomitant LATE-NC and vascular pathology were equally common, and cognition was equally impaired, in PART (Mini-Mental State Examination [MMSE] = 24.8 ± 6.9) and ADNC (MMSE = 24.2 ± 6.0). 5 key findings →
Participants: 45 Evidence: low
Full summary, score breakdown and related studies → Original source
Compared to those without LATE-NC or ADNC, those with pure LATE-NC had a faster decline in global cognition (p = 0.025) and episodic memory (p = 0.002); however, compared to persons with pure ADNC, those with pure LATE-NC showed a slower decline. 5 key findings →
Participants: 378 Evidence: low
Full summary, score breakdown and related studies → Original source
Elderly human brains are vulnerable to multiple proteinopathies, although each protein has a different transmission pathway. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
See Vandenberghe and Schaeverbeke (doi:10.1093/awx065) for a scientific commentary on this article. 3 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
Dementia was associated with dysbiosis characterized by differences in beta diversity and changes in taxonomic composition. 5 key findings →
Participants: 23 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is characterized by senile plaques and neurodegeneration although the neurotoxic mechanisms have not been completely elucidated. 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Clinical trials testing tau-targeting therapies may benefit from using fluid biomarkers to recruit individuals at risk of tau aggregation. 1 key finding →
Participants: 163 Evidence: low
Full summary, score breakdown and related studies → Original source
This study supports that PET- and CSF-related A/T/N profiles can be used to predict accurately the stages of AD neuropathology. 2 key findings →
Participants: 100 Evidence: low
Full summary, score breakdown and related studies → Original source
For the purpose of studying the potential neurobehavioral effects of different human apolipoprotein E (apoE) isoforms produced within the brain, transgenic (TG) mice were generated in which human apoE3 or apoE4 isoforms were under control of an astrocyte-specific, glial fibrillary acidic protein promoter and these TG mice were bred back to apoE knockout (KO) mice. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
We examined 204 decedents of the autopsy component of the Honolulu-Asia Aging Study, a longitudinal cohort study, who had been clinically assessed for dementia. 5 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is characterized by amyloid-beta (Aβ) deposits, which come in myriad morphologies with varying clinical relevance. 5 key findings →
Participants: 74 Evidence: low
Full summary, score breakdown and related studies → Original source
For the CSF-based definition of preclinical AD, if a high specificity is required, our data support the use of Aβ42/ttau rather than using Aβ42 in isolation. 3 key findings →
Participants: 38 Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is characterized by amyloid beta (Aβ) plaques and hyperphosphorylated tau in the brain. 1 key finding →
Participants: 88 Evidence: low
Full summary, score breakdown and related studies → Original source
This study provides evidence that CSF metabolites are associated with AD-related pathology, and many of these associations may be causal. 5 key findings →
Participants: 161 Evidence: low
Full summary, score breakdown and related studies → Original source
A newly developed SV2A radiotracer, 18 F-SynVesT-1, was used in this study to investigate synaptic density and its association with Alzheimer's disease (AD) "A/T/N" biomarkers. 2 key findings →
Participants: 97 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Our findings indicate that tau pathology may play a critical role in pathological angiogenesis, contributing to cerebrovascular lesions and neurodegeneration in AD. 4 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Presence of Alzheimer's pathology in patients with RHI/TES is associated with altered cognitive and biomarker profiles. 5 key findings →
Participants: 154 Evidence: low
Full summary, score breakdown and related studies → Original source
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 →