30,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
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
Saito et al developed a novel amyloid precursor protein (APP) knock-in mouse model (APP NL-G-F ) for Alzheimer's disease (AD) to overcome the problem of overexpression of APP in available transgenic mouse models. 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a severe neurodegenerative disease that requires early diagnosis to manage its progression. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Detection of amyloid-β (Aβ) aggregates contributes to the diagnosis of Alzheimer disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Much testing in medicine is aimed at healthy people to facilitate the early detection of health conditions. 1 key finding →
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
This demonstrates that an AD-like APP processing, yielding to levels of APP, βCTF and Aβ42/Aβ40 ratio similar to those observed in AD patients, are sufficient to rapidly trigger early steps of the amyloidogenic and Tau pathways in vivo. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We propose that there is a reciprocal relationship between APP-CT positioning relative to the membrane and PS1 conformation, suggesting that factors that modulate either APP positioning in the membrane or PS1 conformation could be exploited therapeutically. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The results suggest that Tph2 inactivation influences AβPP processing, at least in the hippocampus, although levels of Aβ are unchanged. 3 key findings →
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
Our objective was to predict HIV-associated neurocognitive disorder (HAND) in HIV-infected people using plasma neuronal extracellular vesicle (nEV) proteins, clinical data, and machine learning. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
These findings provided evidence that neuroinflammation might be involved in the development and progression of cognitive deficits in APP/PS1 mice, suggesting novel intervention and prevention strategies for AD. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
An essential feature of Alzheimer's disease (AD) is implicated in brain energy metabolic impairment that is considered underlying pathogenesis of cognitive impairment. 2 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 30,580 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 30,580 records, built mostly from automated pulls of Europe PMC (64.7% of the library) and OpenAlex (16.6%), 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.
1,037 records (3.4% of the library) are not peer-reviewed — 964 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