Alzheimer disease (AD) is the most common cause of dementia in older individuals (>65 years) and has a long presymptomatic phase. 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.
Alzheimer disease (AD) is the most common cause of dementia in older individuals (>65 years) and has a long presymptomatic phase. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Microglia adopt numerous fates with homeostatic microglia (HM) and a microglial neurodegenerative phenotype (MGnD) representing two opposite ends. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
As an essential component of our innate immune system, the complement system is responsible for our defense against pathogens. 4 key findings →
Evidence: low
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Cerebral amyloid angiopathy is caused by deposition of the amyloid beta protein in the cerebral vasculature. 4 key findings →
Evidence: low
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Elevated blood levels of phosphorylated tau (p-tau) are diagnostic of Alzheimer disease and are associated with the deposition of amyloid-β in the cerebral neuropil. 4 key findings →
Evidence: moderate
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The Alzheimer's Disease Neuroimaging Initiative (ADNI) is a large multi-center study designed to develop optimized methods for acquiring longitudinal neuroimaging, cognitive, and biomarker measures of AD progression in a large cohort of patients with Alzheimer's disease (AD), patients with Mild Cognitive Impairment, and healthy controls. 4 key findings →
Design: longitudinal study Evidence: moderate
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The association of testosterone concentrations with dementia risk remains uncertain. 4 key findings →
Evidence: low
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Improved short-term survival after stroke has necessitated quantifying risk and risk factors of long-term sequelae after stroke (ie, recurrent stroke and dementia). 4 key findings →
Participants: 1,237 Evidence: low
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Transgenic mice carrying disease-linked forms of genes associated with Alzheimer disease often demonstrate deposition of the beta-amyloid as senile plaques and cerebral amyloid angiopathy. 4 key findings →
Evidence: low
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Frontotemporal lobar degeneration with TDP-43 inclusions (FTLD-TDP) is a fatal neurodegenerative disease with no available treatments. 4 key findings →
Evidence: low
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Mitochondrial dysfunction and oxidative stress occur in vascular dementia (VaD), but the specific molecular mechanism regulating these events remains unclear. 4 key findings →
Evidence: low
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Cerebral amyloid angiopathy (CAA) is a cerebrovascular disorder characterized by the deposition of amyloid-β (Aβ) in the walls of leptomeningeal and cortical blood vessels that increases risk of intracerebral hemorrhages and progressive cognitive decline. 2 key findings →
Participants: 251 Evidence: moderate
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These analyses suggest that CenTauR harmonization increases the comparability of tau‐PET data acquired with different tracers. 2 key findings →
Design: longitudinal study Participants: 1,089 Evidence: moderate
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Among 934,792 individuals, 81,731 developed dementia over a mean follow-up of 11·6 years. 1 key finding →
Participants: 934,792 Evidence: low
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We recruited 1501 participants (304 with FTLD, 512 with AD, and 685 healthy controls) from the Multi-Partner Consortium to Expand Dementia Research in Latin America (ReDLat). 5 key findings →
Participants: 1,501 Evidence: low
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Using human stem cell-derived neurons, we show that TDP-43 reduction induces cryptic splicing and downregulation of these genes, resulting in impaired excitability and synaptic transmission. 1 key finding →
Evidence: low
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Patients with trisomy 21 [Down syndrome (DS)] progressively develop amyloid beta-protein (A beta) deposits and then other features of Alzheimer's disease (AD), apparently due to increased gene dosage and thus expression of the beta-amyloid precursor protein.
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Autosomal-dominant Alzheimer's disease has provided significant understanding of the pathophysiology of Alzheimer's disease.
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HRU and payments were overall similar between A4 and LEARN Medicare. 5 key findings →
Design: cohort Participants: 367 Evidence: early
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Relationships between CSF biomarkers but not imaging biomarkers varied by racialized groups. 1 key finding →
Evidence: low
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Accumulating evidence suggests that genetic variants in the SORL1 gene are associated with Alzheimer disease (AD), but a strategy to identify which variants are pathogenic is lacking. 3 key findings →
Evidence: low
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These results suggest a potential link between vascular risk and tau pathology in preclinical AD. 4 key findings →
Evidence: low
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Affective symptoms are of prognostic utility, but interventions to prevent dementia syndromes are limited. 1 key finding →
Evidence: low
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Type 2 diabetes mellitus (T2DM) is a risk factor for Alzheimer disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Deposition of iron in the brain is proposed to play a role in the pathophysiology of the normal aging process and neurodegenerative diseases. 2 key findings →
Design: longitudinal study Evidence: moderate
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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 →