27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Researchers isolated and purified a protein derived from twisted beta-pleated sheet fibrils in cerebrovascular amyloidosis associated with Alzheimer's disease using specific column chromatography and high performance liquid chromatography methods. 3 key findings →
Evidence: low
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Full summary, score breakdown and related studies → Original source Full text may need a subscription
This review summarizes the expression, post-translational modifications, and functions of tau in physiology and pathophysiology. 4 key findings →
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The amyloid precursor protein (APP) plays a crucial role in the pathogenesis of Alzheimer's disease.
Full summary, score breakdown and related studies → Original source Free full text
Along with mounting evidence that gut microbiota and their metabolites migrate endogenously to distal organs, the 'gut-lung axis,' 'gut-brain axis,' 'gut-liver axis' and 'gut-renal axis' have been established. 1 key finding →
Participants: 1,507 Evidence: low
Full summary, score breakdown and related studies → Original source
Traumatic brain injury (TBI), a major cause of persistent cognitive impairment (CI), increases the long-term risk of developing dementia, including Alzheimer's disease (AD). 3 key findings →
Design: longitudinal study Participants: 29 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
This systematic review aims to elucidate the neuropathological basis of the HIDA and psychosis domains, exploring whether distinct proteinopathies and neural circuit dysfunctions are associated with these symptoms. 4 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
MAF supplementation improved cognitive function, especially after 6 months, in elderly people undergoing rehabilitation. 4 key findings →
Design: randomized controlled trial Evidence: low
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From the 144 participants (56.3% female and 43.7% male, with a mean [standard deviation] age of 80.7 [7.7] years), 118 participants were available for final follow-up. 4 key findings →
Design: cohort study Participants: 144 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is the most common form of dementia. 2 key findings →
Design: meta-analysis Evidence: high
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This article discusses how distinct protein aggregates found in various neurodegenerative disorders appear to cause these conditions. 3 key findings →
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Neurogranin (Ng) is a post-synaptic protein that previously has been shown to be a biomarker for synaptic function when measured in cerebrospinal fluid (CSF). 5 key findings →
Participants: 915 Evidence: low
Full summary, score breakdown and related studies → Original source
Huntington's disease is a neurodegenerative disorder caused by an abnormal CAG repeat expansion within exon 1 of the huntingtin gene HTT. 4 key findings →
Participants: 16 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Neurodegenerative diseases likely share common underlying pathobiology. 5 key findings →
Participants: 82,337 Evidence: low
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The blood-brain barrier (BBB) is a complex and dynamic physiological interface between brain parenchyma and cerebral vasculature. 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
The progressive development of Alzheimer disease (AD)-related lesions, such as neurofibrillary tangles (NFT), amyloid deposits and synaptic loss, and the occurrence of microvascular and small macrovascular pathology within the cerebral cortex are conspicuous neuropathologic features of brain aging. 2 key findings →
Design: case-control study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Given that cognitive performance in the A-/T+ group was poorer than in individuals without either pathology, our results suggest that medial temporal lobe tau without cortical amyloid beta may reflect an early stage on the Alzheimer's pathological continuum. 1 key finding →
Participants: 301 Evidence: low
Full summary, score breakdown and related studies → Original source
. Here, to gain deeper insights into the aetiology of different brain diseases, we used specimens from 1,494 unique donors to generate a population-scale single-cell transcriptomic atlas of the human dorsolateral prefrontal cortex, comprising over 6.3 million individual nuclei. 1 key finding →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The cerebrospinal fluid (CSF) signature of reduced amyloid beta 1-42 (Aβ 42 ), elevated total tau (t-tau), and phosphorylated tau181 (p-tau) is important for the early diagnosis of Alzheimer's disease (AD). 1 key finding →
Design: meta-analysis Evidence: high
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The researchers determined the sequences of human tau protein isoforms that feature amino-terminal insertions. 3 key findings →
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This study examined evidence regarding the oxidative stress hypothesis in Alzheimer's disease. 4 key findings →
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Full summary, score breakdown and related studies → Original source Full text may need a subscription
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Patients with Alzheimer disease have reduced levels of sRAGE in plasma compared with patients with vascular dementia and controls. 2 key findings →
Design: cross-sectional Participants: 152 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 →