These results suggest that neuronal injury markers such as VLP-1 may have utility as biomarkers for AD. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Research
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
From a clinical perspective, these data further support the rationale for physicians to provide effective management of CVD risk factors and for patients to be compliant with such recommendations to possibly prevent cognitive decline/dementia. 4 key findings →
Design: open-label trial Evidence: high
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The Montreal Cognitive Assessment (MoCA) is a brief cognitive screening tool with high sensitivity for screening patients with mild cognitive impairment (MCI). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
46/100
The high burden of cognitive impairment in hemodialysis and chronic kidney disease (CKD) patients has only recently become recognized. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Future educational supports for GPs need to be developed which concentrate on these areas. 1 key finding →
Participants: 300 Evidence: low
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Previous studies have suggested that 4 latent constructs (depressed affect, well-being, interpersonal problems, somatic symptoms) underlie the item responses on the Center for Epidemiological Studies Depression (CES-D) Scale. 3 key findings →
Participants: 1,183 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Recent findings Corticobasal degeneration and PSP are neurodegenerative diseases characterized by neuronal loss and gliosis in cardinal brain regions, as well as the abnormal deposition of the microtubule associated protein tau in cell bodies and cell processes. 2 key findings →
Evidence: low
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Adults with Down syndrome (DS) develop Alzheimer neurofibrillary degeneration in the brain, but the underlying molecular mechanism is unknown. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Two groups of tau, 3R- and 4R-tau, are generated by alternative splicing of tau exon 10. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Numerous investigations point to the importance of oxidative imbalance in mediating AD pathogenesis. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We investigated the changes of sulcal shape (average mean curvature in folded regions and sulcal depth) in mild cognitive impairment (MCI) and Alzheimer's disease (AD) using quantitative surface-based methods in a large sample of magnetic resonance imaging data. 4 key findings →
Evidence: low
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46/100
Two-thirds of MCI-multidomains, but only half of MCI-amnestic progress to AD. 1 key finding →
Evidence: low
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Multiple pathogenic factors may contribute to the pathophysiology of Alzheimer's disease (AD). 3 key findings →
Participants: 34 Evidence: low
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Amyloid plaques, composed of the amyloid beta-protein (Abeta), are hallmark neuropathological lesions in Alzheimer disease (AD) brain. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Accumulation of extracellular amyloid beta peptide (Abeta), generated from amyloid precursor protein (APP) processing by beta- and gamma-secretases, is toxic to neurons and is central to the pathogenesis of Alzheimer disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer disease beta-amyloid (Abeta) peptides are generated via sequential proteolysis of amyloid precursor protein (APP) by BACE1 and gamma-secretase. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Beta-amyloid (Abeta) peptides that accumulate in Alzheimer disease are generated from the beta-amyloid precursor protein (betaAPP) by cleavages by beta-secretase BACE1 and by presenilin-dependent gamma-secretase activities. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
A majority of mutations within the beta-amyloid region of the amyloid precursor protein (APP) gene cause inherited forms of intracerebral hemorrhage. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Four themes emerged that relate to stigma in RC-AL: (a) ageism in long-term care; (b) stigma as related to disease and illness; (c) sociocultural aspects of stigma; and (d) RC-AL as a stigmatizing setting. 4 key findings →
Participants: 309 Evidence: low
Full summary, score breakdown and related studies → Original source
These data are evidence of a gene x environment interaction for cognitive aging. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Mucopolysaccharidosis type III (MPS III, Sanfilippo syndrome) is an autosomal recessive disorder, caused by a deficiency in one of the four enzymes involved in the lysosomal degradation of the glycosaminoglycan heparan sulfate. 5 key findings →
Evidence: low
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Dementia caregiving has been associated with negative effects on caregiver health and early nursing home placement for dementia patients. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
The prevalence of idiopathic normal-pressure hydrocephalus (NPH) in a community was investigated by retrospective analysis of data from a previous community-based study of 170 randomly selected elderly residents aged 65 years or older. 1 key finding →
Participants: 170 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
45/100
Caregivers with higher mastery had less NE reactivity to the stressor task. 2 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
45/100
Aging is accompanied by cognitive decline in a major segment of the population and is the primary risk factor for Alzheimer's disease and other prevalent neurodegenerative disorders. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Where “Free full text” comes from
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
How the 0–100 score works — and why some entries are capped
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.
- Journal tier up to 10 pts
- Journal's citation record up to 4 pts
- Study design up to 12 pts
- Strength of evidence up to 5 pts
- Peer-review validation up to 10 pts
- How recent up to 5 pts
- Sample size up to 4 pts
- Effect reported up to 3 pts
- Studied in people up to 3 pts
- Randomised / blinded up to 2 pts
- Times cited up to 7 pts
- Citations per year up to 5 pts
- Impact for its field and year up to 6 pts
- Cited by studies here up to 6 pts
- Still being cited up to 4 pts
- Senior author's track record up to 4 pts
- Institution's track record up to 3 pts
- Multi-centre collaboration up to 3 pts
- Indexed in PubMed up to 2 pts
- Free to read up to 2 pts
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.
What this library is — and isn't
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 →