We conclude that the Aβ 37/42 ratio sensitively detects presenilin/γ-secretase dysfunction and better distinguishes CN from AD than Aβ42/40 in CSF. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
We conclude that the Aβ 37/42 ratio sensitively detects presenilin/γ-secretase dysfunction and better distinguishes CN from AD than Aβ42/40 in CSF. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Energy adjusted niacin intake had a protective effect on development of AD and cognitive decline. 4 key findings →
Participants: 3,718 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The long-term objective of the Rush Memory and Aging Project is to identify the postmortem indices linking genetic and environmental risk factors to the development of Alzheimer's disease (AD). 1 key finding →
Evidence: moderate
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Mechanisms underlying the protective effect of apolipoprotein E ( APOE ) ε2 against Alzheimer’s disease (AD) are not well understood. 4 key findings →
Participants: 982 Evidence: low
Full summary, score breakdown and related studies → Original source
Recent studies indicate that there is a marked reduction in trkA-containing nucleus basalis neurons in end-stage Alzheimer's disease (AD). 4 key findings →
Evidence: moderate
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Florbetapir F 18 selectively binds Aβ in human brain tissue. 4 key findings →
Participants: 40 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Among 428 older autopsied persons (mean age at death = 91 years, 70% women) considered for anti-amyloid treatment eligibility assessment, 58% had MCI and 42% had mild-stage Alzheimer dementia. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Dendritic spine structure is defined by filamentous actin (F-actin) and we observed depolymerization of synaptosomal F-actin accompanied by increased globular-actin (G-actin) at as early as 1 month of age in a mouse model of AD (APPswe/PS1ΔE9, male mice). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Synaptic integrity is now recognized as a central component of Alzheimer's disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We determined whether oxidative stress is an early event in the pathogenesis of sporadic Alzheimer disease (AD), and correlated oxidative stress with neuropsychological functions and neurofibrillary pathology in AD and mild cognitive impairment (MCI). 3 key findings →
Evidence: low
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Transcriptome-wide association studies (TWASs) have been widely used to integrate gene expression and genetic data for studying complex traits. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Atrophy of the hippocampal formation, a region important for the acquisition of new declarative knowledge, has been well-documented in Alzheimer's disease (AD), although the relation of such atrophy to the extent of memory dysfunction in these patients has been less clear. 1 key finding →
Participants: 18 Evidence: low
Full summary, score breakdown and related studies → Original source
Diffusion tensor imaging (DTI) can detect, in vivo, the directionality of molecular diffusion and estimate the microstructural integrity of white matter (WM) tracts. 1 key finding →
Participants: 14 Evidence: low
Full summary, score breakdown and related studies → Original source
Clinical and pathological data from the Rush Memory and Aging Project were used to test the hypothesis that distress proneness is associated with increased risk of Alzheimer's disease (AD). 3 key findings →
Participants: 55 Evidence: low
Full summary, score breakdown and related studies → Original source
Several iPSC-derived three-dimensional (3D) cultures have been generated to model Alzheimer's disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
This influential 2018 paper proposed defining Alzheimer's disease by what is happening biologically in the brain (amyloid plaques, tau tangles, and neuron loss, measured by scans or spinal fluid tests) instead of by memory symptoms alone. 4 key findings →
Evidence: high
Full summary, score breakdown and related studies → Original source
Several recent studies indicate that activity of cholinergic enzymes in the cortex of people with mild cognitive impairment (MCI) and early Alzheimer's disease (AD) are preserved. 3 key findings →
Evidence: low
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A multitiered strategy was adopted to assess tau conformational changes within fibrillar lesions during the progression of Alzheimer's disease (AD). 3 key findings →
Evidence: low
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Alzheimer's disease (AD) is a progressive amnestic dementia that involves post-translational hyperphosphorylation, enzymatic cleavage, and conformational alterations of the microtubule-associated protein tau. 1 key finding →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
The suprachiasmatic nucleus (SCN) of the hypothalamus, the master mammalian circadian pacemaker, synchronizes endogenous rhythms with the external day-night cycle. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Large-scale 'omic' studies investigating the pathophysiological processes that lead to Alzheimer's disease (AD) dementia have identified an increasing number of susceptibility genes, many of which are poorly characterized and have not previously been implicated in AD. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Numerous reports have linked extremity muscle strength with mortality but the mechanism underlying this association is not known. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
With high resolution, quantitative magnetic resonance imaging (MRI) techniques, it is now possible to examine alterations in brain anatomy in vivo and to identify regions affected in the earliest stages of Alzheimer's disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Using quantitative structural MRI protocols, we examined the effects of age on alterations in entorhinal cortex (EC) volume. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The concept of amnestic mild cognitive impairment (MCI) describes older people who show a decline predominantly in memory function, but who do not meet criteria for dementia. 5 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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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.
1,034 records (3.7% 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 →