27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
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
Dogs develop cognitive decline and a progressive accumulation of oxidative damage. 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
A genetic classification of Alzheimer disease(s) (AD) is presented. 4 key findings →
Evidence: low
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Research on cognitive impairment (CI) has increasingly focused on the central nervous system, identifying numerous neuronal targets and circuits of relevance for CI pathogenesis and treatment. 1 key finding →
Design: systematic review Evidence: low
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One of the major histopathological hallmarks of Alzheimer's disease (AD) is redundant senile plaques mainly composed of beta-amyloid (Abeta) aggregates. 5 key findings →
Participants: 19 Evidence: low
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The 4.2-kilodalton (kDa) polypeptide associated with the cerebral amyloid deposits of Alzheimer's disease (AD) derives from a much larger protein that is encoded by a gene on chromosome 21. 4 key findings →
Evidence: low
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Doubly transgenic mice expressing both a mutated amyloid precursor protein and a mutated presenilin-1 protein accumulate A(beta) deposits as they age. 4 key findings →
Evidence: low
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Alzheimer disease (AD) is the most prevalent cause of dementia in humans, and the symptoms are commonly manifested after the seventh decade of life. 4 key findings →
Evidence: low
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Triggering receptor expressed on myeloid cells 2 (TREM2) is cell surface transmembrane receptor of the TREM family, predominantly expressed on microglia within the central nervous system (CNS). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Overactivated microglia and neuroinflammation are considered to play a crucial role in the progression of Alzheimer's disease (AD). 4 key findings →
Evidence: low
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Microglia-mediated neuroinflammation is widely associated with seizures and epilepsy. 4 key findings →
Evidence: low
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Triggering receptor expressed on myeloid cells-2 (TREM2) was a newly identified receptor expressed on microglia. 4 key findings →
Evidence: low
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The complement protein, C1q, has been shown to bind to fibrillar beta-amyloid, resulting in the activation of the classical complement pathway. 4 key findings →
Evidence: low
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We compared lesions in elderly transgenic (tg) mice carrying the Swedish double mutation KM670/671NL with lesions in Alzheimer disease (AD) by histochemical and immunohistochemical techniques. 4 key findings →
Evidence: low
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A multitiered strategy was adopted to assess tau conformational changes within fibrillar lesions during the progression of Alzheimer's disease (AD). 3 key findings →
Evidence: low
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Tau pathology is essential in the pathogenesis of Alzheimer's disease (AD) and related tauopathies. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease is the most prevalent tauopathy and cause of dementia. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a progressive brain disorder characterized by memory loss and the accumulation of two insoluble protein aggregates, tau neurofibrillary tangles and beta-amyloid plaques. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Epidemiological and experimental studies have suggested that high dietary intake of fats is associated with cognitive decline and a significantly increased risk of dementia. 4 key findings →
Evidence: low
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Age and estrogen treatment influenced fiber outgrowth and compensatory neuronal sprouting after unilateral entorhinal cortex lesions (ECL) which model Alzheimer disease-like deafferentation in the dentate gyrus of the hippocampus. 2 key findings →
Evidence: low
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Parkinson's disease (PD), a progressive neurodegenerative disease, results in abnormal accumulation of insoluble alpha-synuclein (alpha-Syn) in dopaminergic neurons. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In vivo imaging of patients with Alzheimer's disease using positron emission tomography (PET) demonstrates progressive reductions in brain glucose metabolism and blood flow in relation to dementia severity, more so in association than primary cortical regions. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The neurofibrillary-tangles (NTFs), characteristic of tauopathies including Alzheimer's-disease (AD), are the pathological features which correlate best with dementia. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Traumatic brain injury (TBI) is a global problem reaching near epidemic numbers that manifests clinically with cognitive problems that decades later may result in dementias like Alzheimer's disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Life's Journey If life is indeed a journey, then poetry must be the map that reveals all its topographic possibilitiesellipsis while science is the compass that keeps us from getting lost. -R. T. Bartus, Simple Words for Complex Lives, (c) 1998 In the nearly 20 years since the cholinergic hypothesis was initially formulated, significant progress has been achieved. 2 key findings →
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 →