28,980 Alzheimer's and dementia studies in plain English, each scored out of 100.
[3H]inositol(1,4,5)-trisphosphate (IP3) binding studies have shown decreased [3H]IP3 binding to brain tissue in several neurodegenerative diseases, including Alzheimer's and Huntington's diseases. 2 key findings →
Evidence: low
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Neuropeptide Y (NPY)-containing neurons are depleted in the cortices of individuals with Alzheimer disease (AD), yet spared in the striatum of patients with Huntington chorea. 2 key findings →
Evidence: low
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A blind study was set up to examine the in vitro growth characteristics of skin fibroblasts from 2 individuals with and 9 at risk for familial Alzheimer disease, 4 individuals with sporadic Alzheimer disease, 18 with Down syndrome as well as 5 younger and 6 older controls. 5 key findings →
Evidence: low
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Regulator of calcineurin 1 (RCAN1) is related to the expression of human neurologic disorders such as Down syndrome, Alzheimer disease, and chromosome 21q deletion syndrome. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Numerous intraneuronal neurofibrillary tangles and senile (neuritic) plaques are the two characteristic lesions in Alzheimer disease (AD) and adult Down syndrome (DS). 4 key findings →
Evidence: low
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Down syndrome (DS) is the most common chromosomal aberration and genetically determined cause of intellectual disability. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Recent evidences indicate that polymorphisms within the promoter region of the vascular endothelial growth factor (VEGF) gene may elevate the risk for Alzheimer's disease (AD). 4 key findings →
Evidence: low
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Most remarkably, research by Cryan and others has shown that transplanting microbes from the guts of people with psychiatric disorders like depression to the guts of rodents can cause comparable symptoms in the animals.CREDIT: JAMES PROVOST (CC BY-ND)Neuroscientist John CryanUniversity College CorkThese effects may occur in several ways — through the vagus nerve connecting the gut to the brain, through the influence of gut bacteria on our immune systems, or by microbes synthesizing molecules that our nerve cells use to communicate. 5 key findings →
Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Our study unveils the complex interplay between area deprivation and language decline in AD patients. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Anemia and iron deficiency are common in older adults, yet their relevance to blood biomarkers for Alzheimer disease (AD) remains underappreciated. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer disease (AD) is the leading cause of dementia globally and is defined by the presence of amyloid-β (Aβ) plaques and neurofibrillary tangles formed by the accumulation of phosphorylated tau (p-tau). 2 key findings →
Evidence: low
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The pathological activation of AD microglia significantly amplifies endogenous aging characteristics. 4 key findings →
Evidence: low
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Vascular dementia (VaD), a primary cognitive disorder caused by cerebrovascular pathology, features significant white matter damage from chronic cerebral hypoperfusion strongly correlated with cognitive decline. 1 key finding →
Evidence: low
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Tauopathies are a group of neurodegenerative disorders, including Alzheimer's disease, frontotemporal dementia, and progressive supranuclear palsy, characterized by the pathological accumulation of tau protein. 1 key finding →
Evidence: low
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hONE-NPCs expressed proteins such as Ki67, Nestin, GFAP, and b-III Tubulin, which are associated with cellular proliferation and the neuronal progenitor lineage. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In Transmissible Spongiform Encephalopathies (TSEs) and Alzheimer disease (AD) both misfolding and aggregation of specific proteins represent key features. 2 key findings →
Evidence: low
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Recent data have allowed speculating that amyloid Aβ induces apoptosis via opening type-1 VDAC in cell membranes of hypo-metabolic neurons, a process most likely running over life time--as leaves fall from trees in the tropics--and ending in Alzheimer's disease whenever critical brain regions are affected. 5 key findings →
Evidence: low
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Patients with Down syndrome (human trisomy 21) develop neuropathological and cholinergic functional defects characteristic of Alzheimer's disease, which has been attributed to the location of the Alzheimer beta-amyloid precursor protein on chromosome 21. 4 key findings →
Evidence: low
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In humans, GART [phosphoribosylglycinamide formyltransferase (EC 2.1.2.2) / phosphoribosylglycinamide synthetase (EC 6.3.4.13) / phosphoribosylaminoimidazole synthetase (EC 6.3.3.1)] is a trifunctional protein which catalyzes the second, third, and fifth reactions of the ten step de novo purine synthesis (DNPS) pathway. 4 key findings →
Evidence: low
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A Doença de Alzheimer (DA) é uma das condições neurodegenerativas mais prevalentes do Sistema Nervoso Central (SNC), caracterizada pelo acúmulo anormal de placas beta-amilóide (Aβ) e emaranhados neurofibrilares, levando à degeneração neuronal e ao comprometimento progressivo das funções cognitivas. 5 key findings →
Evidence: low
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Alzheimer-Perusini's disease (AD) represents a growing health crisis. 5 key findings →
Evidence: low
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Alzheimer’s disease (AD) is the most widespread neurodegenerative disorder and a leading cause of dementia seen in clinical practice. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
As a result of multiple phosphorylation, Tau undergoes early conformational changes involving the bending of the intact amino (N)-terminus over the third repeated domain, which in turn was evidenced by positive immunolabeling with the monoclonal antibody Alz-50 [2]. 4 key findings →
Evidence: low
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Alzheimer disease (AD) is a major health issue of global concern whereby there are minimal treatment options. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Social isolation (SI) and loneliness (perceived social isolation) are considered as risk factors for developing dementia, including Alzheimer's disease (AD), in the elderly population. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
10 of the 7,799 studies in this tag that have a study page, 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 28,980 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 28,980 records, built mostly from automated pulls of Europe PMC (62.8% of the library) and OpenAlex (17.6%), 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.
1,038 records (3.6% of the library) are not peer-reviewed — 966 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 →