27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Adding MDLC to p-tau217 significantly explained longitudinal cognitive trajectory beyond p-tau217 alone. 5 key findings →
Design: longitudinal study Participants: 183 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Across the cohorts, each 10-year increase in BAI was associated with a 39% higher risk of incident dementia (hazard ratio [HR], 1.39 [95% CI, 1.21-1.59]; P Conclusions and relevance In this IPD meta-analysis, a higher sleep EEG-based BAI was associated with a higher risk of incident dementia. 3 key findings →
Design: meta-analysis Participants: 7,105 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
We established AD diagnostic models using plasma biomarkers for Chinese participants. 2 key findings →
Participants: 159 Evidence: low
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This approach offers a sensitive method for identifying individuals at high risk for AD-related cognitive decline. 1 key finding →
Participants: 954 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Clinical symptoms correlate with underlying neurodegenerative changes in the vast majority of people. 3 key findings →
Participants: 14 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Elevated microglial activation in the right amygdala-entorhinal-hippocampal complex of App NL-G-F mice is associated with better spatial learning. 5 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Models including plasma biomarkers yielded the most accurate predictions of tau-PET burden (best model: R-squared = 0.66-0.69), with especially high contribution from plasma phosphorylated tau-217 (p-tau217). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
As the population ages, neurodegenerative diseases are becoming more prevalent, making it crucial to comprehend the underlying disease mechanisms and identify biomarkers to allow for early diagnosis and effective screening for clinical trials. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Quantification results using the proposed deep learning-based method showed stronger correlations with the FreeSurfer estimates than SPM-based SN using MRI did. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
These results suggest that the targeted methylation of APP via dCas9-Dnmt3a treatment can be a potential therapeutic strategy for AD. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
App NL/NL and App NL-G-F/NL-G-F mice exhibit behavioral changes associated with non-cognitive, emotional domains before the onset of definitive cognitive deficits. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid pathology occurs early in Alzheimer's disease (AD), and has therefore been the focus of numerous studies. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We have shown that chronically administered cannabinoid showed marked beneficial effects concomitant with inflammation reduction and increased Aβ clearance. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The combination of the scaffolds of the cholinesterase inhibitor huprine Y and the antioxidant capsaicin results in compounds with nanomolar potencies toward human acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) that retain or improve the antioxidant properties of capsaicin. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Pathological amino-acid substitutions in the amyloid precursor protein (APP) and chemical γ-secretase modulators affect the processing of APP by the γ-secretase complex and the production of the amyloid-beta peptide Aβ42, the accumulation of which is considered causative of Alzheimer's disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cleavage of the amyloid precursor protein's (APP) transmembrane domain (TMD) by γ-secretase is a crucial step in the aetiology of Alzheimer's Disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Inexpensive, non-invasive tools for assessing Alzheimer-type pathophysiologies are needed. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The search for new therapeutic approaches to Alzheimer disease (AD) is a major goal in medicine and society, also due to the impressive economic and social costs of this disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Monitoring the ratio of 40- and 42-residue amyloid β peptides (i.e., Aβ40 and Aβ42) in human plasma is considered one of the hallmarks of detection of the early stage of Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We suggest a one-step quantification method for amyloid PET via a deep learning model. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The accumulation of aggregated amyloid-β (Aβ) in amyloid plaques is a neuropathological hallmark of Alzheimer's disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In both trisomy 21 and rare cases of triplication of amyloid precursor protein (APP) Alzheimer's disease (AD) pathological changes are believed to be secondary to increased expression of APP. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Hypertension (HTN) doubles the risk of Alzheimer’s disease (AD), but the mechanisms remain unclear. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
A growing body of epidemiological evidence suggests that fruit and vegetable juices containing various phenolic compounds can reduce the risk of Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) beta-amyloid peptide (Abeta and betaA4) is derived from the amyloid precursor protein (APP) by the subsequent action of the so-far unidentified beta- and gamma-secretases. gamma-secretase, which generates the C-terminus of Abeta, cleaves within the transmembrane domain of APP, preferentially after Abeta-residue 40 (Abeta 40) but also after residue 42 (Abeta 42). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
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 →