27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Emerging evidence indicates that impaired mitophagy-mediated clearance of defective mitochondria is a critical event in Alzheimer's disease (AD) pathogenesis. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
APOE4 genotype is the strongest genetic risk factor for Alzheimer's disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is the most common cause of dementia, yet there is no cure or diagnostics available prior to the onset of clinical symptoms. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Microglia are active modulators of Alzheimer's disease but their role in relation to amyloid plaques and synaptic changes due to rising amyloid beta is unclear. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Integrative gene network approaches enable new avenues of exploration that implicate causal genes in sporadic late-onset Alzheimer's disease (LOAD) pathogenesis, thereby offering novel insights for drug-discovery programs. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Amyloid-β (Aβ) deposits are a relatively late consequence of Aβ aggregation in Alzheimer's disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Carriers of the e4 allele may be more vulnerable to conditions that are independent risk factors for cognitive decline, such as cardiometabolic diseases. 4 key findings →
Participants: 111,739 Evidence: low
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Alzheimer's disease is the commonest dementia. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is the most prevalent form of late-onset dementia. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer disease (AD) is a frequent and devastating neurodegenerative disease in humans, but still no curative treatment has been developed. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Microglial activation is a key feature in Alzheimer's disease and is considered to contribute to progressive neuronal injury by release of neurotoxic products. 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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For years, it has been reported that Alzheimer's disease (AD) is the most common cause of dementia. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is a devastating neurodegenerative disorder and a leading cause of dementia, with accumulation of amyloid-beta (Aβ) and neurofibrillary tangles (NFTs) as defining pathological features. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) and Parkinson's disease (PD) are the two common neurodegenerative diseases characterized by progressive neuronal dysfunction in the presence of pathological microglial activation. 4 key findings →
Evidence: low
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Brain iron accumulation has been found to accelerate disease progression in amyloid-β(Aβ) positive Alzheimer patients, though the mechanism is still unknown. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) diagnosis relies on cerebrospinal fluid (CSF) biomarkers or amyloid PET. 1 key finding →
Participants: 134 Evidence: low
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Stroke interacts with APOE ε4 to influence dementia, with the association being more pronounced in APOE ε4 non‐carriers. 4 key findings →
Design: cohort study Participants: 336 Evidence: moderate
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Latin America’s diverse genetic landscape provides a unique opportunity to study Alzheimer’s disease (AD) and frontotemporal dementia (FTD). 1 key finding →
Participants: 2,162 Evidence: low
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In amyloid PET–positive MCI, Ginkgo biloba use was associated with sustained clinical stability, reduced plasma Aβ oligomerization tendency, and attenuation of amyloid PET progression over 18 months. 2 key findings →
Design: cohort study Participants: 21 Evidence: moderate
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-heterozygous human brain tissue was reactivated in response to neuroinflammation caused by exposure to other pathogens. 2 key findings →
Evidence: low
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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
In mild AD patients aged less than 75 years, the mean age-at-diagnosis of AD in APOE4 carriers was reduced by over 6 years in BCHE-K carriers versus noncarriers. 5 key findings →
Participants: 33 Evidence: low
Full summary, score breakdown and related studies → Original source
Our findings suggest that the proposition that synaptic markers can predict cognitive decline in AD, should be extended to Lewy body diseases. 4 key findings →
Participants: 129 Evidence: low
Full summary, score breakdown and related studies → Original source
Astrocytes contribute to a variety of functions in the brain, including homeostasis, synapse formation, plasticity, and metabolism. 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
10 of the 1,344 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
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 →