Cerebral deposition of the amyloid beta protein (A beta) is an early and invariant feature of Alzheimer disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Cerebral deposition of the amyloid beta protein (A beta) is an early and invariant feature of Alzheimer disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The common inhalation anesthetic isoflurane has previously been reported to enhance the aggregation and cytotoxicity of the Alzheimer disease-associated amyloid beta protein (Abeta), the principal peptide component of cerebral beta-amyloid deposits. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Mutations in the presenilin 1 (PS1) and presenilin 2 (PS2) genes increase the production of the highly amyloidogenic 42-residue form of amyloid beta-protein (Abeta42) in a variety of cell lines and transgenic mice. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Understanding the mechanisms of amyloid-beta protein (Abeta) production and clearance in the brain has been essential to elucidating the etiology of Alzheimer disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Late-onset Alzheimer's disease (AD) is a sporadic disorder with increasing prevalence in aging. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The clinical progression of Alzheimer disease (AD) is associated with the accumulation of tau neurofibrillary tangles, which may spread throughout the cortex by interneuronal tau transfer. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We review the implications of the recently approved aducanumab amyloid-β immunotherapy for treating Alzheimer disease with comorbid cerebral amyloid angiopathy. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
This study investigated whether patients with mild to moderately severe dementia or possible Alzheimer's disease (AD) with Mini-Mental State Exam (MMSE) Baseline scores of 10-24 would improve when treated with near-infrared photobiomodulation (PBM) therapy. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The interstitial fluid (ISF) drainage pathway has been hypothesized to underlie the clearance of solutes and metabolites from the brain. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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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In 2014 and 2016, the overall prevalence of AD/ADRD diagnoses was 5.6% and 6.5%, respectively. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Prior authorization criteria for Federal Drug Administration (FDA) approved immunotherapeutics, among the class of anti-amyloid monoclonal antibodies (mAbs), established by state drug formulary committees, are tailored for adults with late-onset Alzheimer's disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Midlife hearing loss was associated with smaller brain volumes, accelerated decline in executive function, accelerated accrual of white matter abnormalities, and a near doubling of dementia risk, suggesting a potential causal or biomarker role for midlife hearing loss in the prevention of late‐life dementia. 4 key findings →
Participants: 1,656 Evidence: low
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Among 52 participants recruited, 27 were former caregivers, 16 were current caregivers, and nine were persons with dementia; experiences reflected Alzheimer's (n = 18), sporadic Creutzfeldt-Jakob (n = 12), Lewy body (n = 7), and other dementias (n = 15). 5 key findings →
Participants: 18 Evidence: low
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White matter hyperintensities (WMH) are neuroimaging markers linked to an elevated risk of cognitive decline. 2 key findings →
Participants: 60 Evidence: low
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In 3413 participants (mean age: 59 ± 14 years, 53.4% women), 11% had prevalent CVD or AF, 8% had prevalent CVD, and 4% had prevalent AF. 5 key findings →
Participants: 3,413 Evidence: moderate
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Genome-wide association studies have led to numerous genetic loci associated with Alzheimer's disease (AD). 2 key findings →
Participants: 2,247 Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid PET imaging is a novel diagnostic test that can detect in living humans one of the two defining pathologic lesions of Alzheimer disease, amyloid-β deposition in the brain. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Growing evidence supports a strong and likely causal association between cardiovascular disease (CVD), and its risk factors, with incidence of cognitive decline and Alzheimer's disease. 1 key finding →
Evidence: low
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Accumulating studies suggest that overnutrition-associated obesity may lead to development of type 2 diabetes mellitus and metabolic syndromes (MetS). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
This article outlines methodological enhancements to better evaluate treatment approaches in future registration trials and provides an algorithm for improving the treatment of these patients in nursing home and non-nursing home settings. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The median age of participants was 79 years, 69% (31 of 45) were of non-Hispanic white race/ethnicity, and 60% (27 of 45) had attended at least some college. 2 key findings →
Evidence: low
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A common but significant change associated with aging is a profound disruption to the daily sleep-wake cycle. 3 key findings →
Evidence: low
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Amyloid-β (Aβ) peptides, starting with pyroglutamate at the third residue (pyroGlu-3 Aβ), are a major species deposited in the brain of Alzheimer disease (AD) patients. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Adults with Down syndrome (DS) have an exceptionally high prevalence of Alzheimer disease (AD), with an earlier age of onset compared with the neurotypical population. 4 key findings →
Participants: 339 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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 →