27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Although possession of the APOE epsilon4 allele is a risk factor for AD in old age, it does not modify the progression of the disease during the preclinical period. 1 key finding →
Evidence: low
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Individuals over 50 years of age comprise 11% of AIDS cases reported to the Centers for Disease Control and Prevention. 2 key findings →
Design: cohort study Evidence: moderate
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Alzheimer's disease is characterized both by a lower mean level of functional connectivity as well as by diminished fluctuations in the level of synchronization. 2 key findings →
Participants: 24 Evidence: low
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Insulin is best known for its action on peripheral insulin target tissues such as the adipocyte, muscle and liver to regulate glucose homeostasis. 3 key findings →
Evidence: low
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This paper reviews current knowledge on sleep problems, sleep architecture changes and quantitative EEG alteration brought on by various neurodegenerative diseases, such as Alzheimer's disease (AD), progressive supranuclear palsy (PSP), REM sleep behavior disorder (RBD), Parkinson's disease (PD), dementia with Lewy bodies (DLB), multiple system atrophy MSA, Huntington's disease and Creutzfeldt-Jakob disease, in comparison to normal aging. 2 key findings →
Evidence: low
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Cytoplasmic deposition of alpha-synuclein aggregates is a common pathological feature of many neurodegenerative diseases. 2 key findings →
Evidence: low
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Inhibition of gamma-secretase, one of the enzymes responsible for the cleavage of the amyloid precursor protein (APP) to produce the pathogenic beta-amyloid (Abeta) peptides, is an attractive approach to the treatment of Alzheimer disease. 4 key findings →
Evidence: low
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Evidence suggests that Alzheimer disease (AD) begins as a disorder of synaptic function, caused in part by increased levels of amyloid beta-peptide 1-42 (Abeta42). 4 key findings →
Evidence: low
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Increasing evidence points to synaptic plasticity impairment as one of the first events in Alzheimer's disease (AD). 4 key findings →
Evidence: low
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CSF Abeta42 was significantly lower and CSF total tau and CSF Ptau-181 significantly higher in EAD patients than FTLD patients and control subjects. 4 key findings →
Evidence: low
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Myeloperoxidase, a heme protein expressed by professional phagocytic cells, generates an array of oxidants which are proposed to contribute to tissue damage during inflammation. 4 key findings →
Evidence: low
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Using positron emission tomography and [(11)C](R)-PK11195, a marker of "peripheral benzodiazepine sites" that is upregulated on activated microglia during progressive tissue pathology, we show increased binding of [(11)C](R)-PK11195 in frontotemporal lobar degeneration in the typically affected frontotemporal brain regions. 2 key findings →
Evidence: low
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Our aim was to investigate the long-term prognosis of delirium in the frailest elderly, and to clarify whether delirium is just a marker of the underlying severe disease. 5 key findings →
Participants: 425 Evidence: low
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Diabetic patients are at increased risk for stroke, but little is known about the presence of other brain lesions. 3 key findings →
Participants: 1,252 Evidence: low
Full summary, score breakdown and related studies → Original source
To address this, we first examined the prevalence of type 2 diabetes in a community-based controlled study, the Mayo Clinic Alzheimer Disease Patient Registry (ADPR), which follows patients with Alzheimer disease versus control subjects without Alzheimer disease. 2 key findings →
Participants: 100 Evidence: moderate
Full summary, score breakdown and related studies → Original source
In this study, the authors evaluated whether the association between low educational level and increased risk of Alzheimer's disease (AD) and dementia may be explained by occupation-based socioeconomic status (SES). 5 key findings →
Participants: 101 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The incidence of hip fracture appears to be associated with benzodiazepine use. 3 key findings →
Participants: 125 Evidence: moderate
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Energy adjusted niacin intake had a protective effect on development of AD and cognitive decline. 4 key findings →
Participants: 3,718 Evidence: low
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To better understand the pathogenesis of brain dysfunction in Gaucher disease (GD), we studied brain pathology in seven subjects with type 1 GD (four also exhibited parkinsonism and dementia), three with type 2 GD and four with type 3 GD. 3 key findings →
Evidence: low
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Degeneration of cholinergic nucleus basalis (NB) cortical projection neurons is associated with cognitive decline in late-stage Alzheimer's disease (AD). 3 key findings →
Evidence: low
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Anti-Abeta immunotherapy in transgenic mice reduces both diffuse and compact amyloid deposits, improves memory function and clears early-stage phospho-tau aggregates. 4 key findings →
Evidence: low
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Accumulation of amyloid beta-peptide (Abeta) in the central nervous system (CNS) may initiate pathogenic cascades mediating neurovascular and neuronal dysfunctions associated with the development of cerebral beta-amyloidosis and cognitive decline in patients with Alzheimer disease (AD) and with related familial cerebrovascular disorders. 3 key findings →
Evidence: low
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Several proteins are expressed in both immune and nervous systems. 4 key findings →
Evidence: low
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Though cerebral white matter injury is a frequently described phenomenon in aging and dementia, the cause of white matter lesions has not been conclusively determined. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Atlas normalization, as commonly used by functional data analysis, provides an automated solution to the widely encountered problem of correcting for head size variation in regional and whole-brain morphometric analyses, so long as an age- and population-appropriate target atlas is used. 2 key findings →
Participants: 49 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 →