27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
The amyloid precursor protein (APP) plays a central role in Alzheimer disease (AD) pathogenesis because sequential cleavages by beta- and gamma-secretase lead to the generation of the amyloid-beta (Abeta) peptide, a key constituent in the amyloid plaques present in brains of AD individuals. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The AD subjects showed positive correlations between CSF-T-tau and CSF-P-tau versus CSF-Mn (r(s) = 0.22, p = 0.004; r(s) = 0.18, p = 0.021). 4 key findings →
Participants: 264 Evidence: low
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It is widely known that exogenous formaldehyde exposure induces human cognitive impairment and animal memory loss; and recent studies show that formaldehyde at pathological levels induces Aβ deposition and misfolding of tau protein to form globular amyloid-like aggregates. 4 key findings →
Participants: 141 Evidence: low
Full summary, score breakdown and related studies → Original source
Human immunodeficiency virus type 1 (HIV-1) infection of the central nervous system (CNS) can result in neurological dysfunction with devastating consequences in a significant proportion of individuals with acquired immune deficiency syndrome. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
(18)F-flutemetamol uptake can be readily quantified. 3 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
This observational study revealed that the addition of the NMDA receptor antagonist memantine to the treatment of AD with ChEI significantly altered the treated history of AD by extending time to nursing home admission. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloids are highly organized cross-beta-sheet-rich protein or peptide aggregates that are associated with pathological conditions including Alzheimer's disease and type II diabetes. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Mitochondria continuously undergo two opposing processes, fission and fusion. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Profound neuronal dysfunction in the entorhinal cortex contributes to early loss of short-term memory in Alzheimer's disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The three human alleles of apolipoprotein E (APOE) differentially influence outcome after CNS injury and affect one's risk of developing Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The past 30 years have seen multiple attempts at demonstrating the safety and efficacy of drugs for Alzheimer's disease (AD), predominantly to improve symptoms. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
No treatment effect on GSK-3 activity or CSF-based biomarker concentrations (P >. 05) was observed. 4 key findings →
Participants: 38 Evidence: low
Full summary, score breakdown and related studies → Original source
Test-retest reliability data of the Arabic MoCA were collected approximately 35.0 +/- 17.6 days apart. 2 key findings →
Evidence: low
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The white matter (WM) of the adult human neocortex contains the so-called "interstitial neurons". 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In order to explore the impact of a degraded semantic system on the structure of language production, we analysed transcripts from autobiographical memory interviews to identify naturally-occurring speech errors by eight patients with semantic dementia (SD) and eight age-matched normal speakers. 2 key findings →
Evidence: low
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Hyperhomocysteinemia and beta-amyloid (Abeta) overproduction are critical etiological and pathological factors in Alzheimer disease, respectively; however, the intrinsic link between them is still missing. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Retinal ganglion cell loss is considered to be a cause of visual impairment in Alzheimer;s patients. 4 key findings →
Evidence: low
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Synapse loss is an early and invariant feature of Alzheimer's disease (AD) and there is a strong correlation between the extent of synapse loss and the severity of dementia. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) and Parkinson's disease (PD) are the most common causes of dementia and movement disorders in the elderly. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Aging is associated with cognitive decline, yet this does not prevent older adults from finding ways to compensate for age-related deficits. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Medications with anticholinergic activity negatively affect the cognitive performance of older adults. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Most feeding tubes are inserted in an acute care hospital. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Delirium was associated with increased level of S100B which could indicate cerebral damage either due to delirium or leading to delirium. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The authors identified 2 Class I studies, 8 Class II studies, and 30 Class III studies in ALS, but many important areas have been little studied. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
These findings indicate that among Lewy body disease cases that pass through a mild cognitive impairment stage, any cognitive pattern or mild cognitive subtype is possible, with the attention/executive and visuospatial domains most frequently impaired. 1 key finding →
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 →