27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Long non-coding RNAs (lncRNAs) are increasingly recognized as regulators of brain cell function, but their roles in astrocyte biology and neurodegeneration remain poorly understood. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Aberrant alternative splicing alters multiple disease-associated splicing events, including MAPT exon 10 inclusion linked to tau pathology, and thereby impacts Alzheimer’s disease (AD) progression. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The accumulation of tau tangles and Aβ plaques are prominent neuropathologies that characterize Alzheimer’s disease (AD) and Down Syndrome (DS). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) and Down Syndrome (DS) are characterized by the aggregation of tau tangles. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Mitochondrial dysfunction, oxidative stress, neuroinflammation, and impaired protein homeostasis form interconnected pathological networks in acute central nervous system injury and chronic neurodegenerative disease. 5 key findings →
Design: narrative review Evidence: low
Full summary, score breakdown and related studies → Original source
SGLT2 inhibitors and GLP-1 receptor agonists have the greatest effect on cognition in T2DM, and the multi-component exercise as the most effective lifestyle component. 3 key findings →
Design: meta-analysis Participants: 213,604 Evidence: high
Full summary, score breakdown and related studies → Original source
Capturing the systemic effects of drugs in vivo remains a fundamental challenge for drug repurposing strategies. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We describe the demographic and clinical characteristics of new initiators of GLP-1RAs compared with initiators of alternative therapies, including sodium-glucose cotransporter-2 inhibitors (SGLT2i) and dipeptidyl peptidase-4 inhibitors (DPP-4i). 5 key findings →
Design: retrospective cohort Participants: 58,754 Evidence: moderate
Full summary, score breakdown and related studies → Original source
GLP-1 agonist drug repurposing efforts may establish new clinical niches in managing psychiatric and neurological disorders. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
These findings reinforce the potential of GLP-1RAs and SGLT2i as therapeutic options to slow cognitive decline in DM2, possibly depending on glycemic control and central modulation. 5 key findings →
Design: cohort study Participants: 12 Evidence: high
Full summary, score breakdown and related studies → Original source
Glucagon-like peptide-1 receptor agonists (GLP-1 RAs) have moved rapidly from metabolic medicine into neurology, but the evidence to mid-2026 refuses to resolve into a single narrative of neuroprotection. 5 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Four distinct subtypes were identified: I low-risk healthy aging, II behavioral/social vulnerability, III cardiometabolic–depressive multimorbidity, and IV mixed social-medical vulnerability profiles. 5 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source
In propensity-matched comparator analyses, during the 2 year time-period from treatment initiation, semaglutide was associated with broadly lower neuropsychiatric event risk than metformin, SGLT2 inhibitors, and DPP-4 inhibitors. 4 key findings →
Design: longitudinal study Participants: 63,215 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Individuals who carry two copies of the apolipoprotein E ε4 ( APOE ε4) allele are at high risk of developing Alzheimer’s disease (AD), yet the effects of APOE ε4 homozygosity on biological pathways related to AD over the lifespan are unknown. 1 key finding →
Participants: 413 Evidence: low
Full summary, score breakdown and related studies → Original source
EVOKE and EVOKE+ trials showed no population-level slowing of early symptomatic Alzheimer’s disease (AD) with semaglutide, motivating an assessment of whether clinical-note phenotyping over decades of routine care could identify distinct AD trajectories. 3 key findings →
Participants: 2,169 Evidence: low
Full summary, score breakdown and related studies → Original source
Eligible studies reported MACE or dementia outcomes in adults ≥ 50 years for at least one of three intervention classes (RZV, SGLT2i, GLP-1 RA) versus placebo or active comparator, with follow-up ≥ 6 months. 5 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source
Glucagon-like peptide-1 receptor agonists (GLP-1 RAs) have shown promise in preclinical models of neurodegeneration, with emerging evidence suggesting these effects may be driven by modulation of neuroinflammation. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease continues to be one of the major critical neurodegenerative ailments of the modern era, with acetylcholinesterase (AChE) inhibition standing as a foundational therapeutic strategy. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder that is the leading cause of dementia in older people. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a progressive neurodegenerative condition marked by cognitive decline, memory loss, and cholinergic dysfunction [1]. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Approved Alzheimer’s disease therapies fail to address the two drivers of cognitive decline: loss of BDNF-TrkB signalling and accumulation of hyperphosphorylated tau protein. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Galantamine is a pharmaceutically relevant Amaryllidaceae alkaloid used for the treatment of Alzheimer’s disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
This study reports the eco-friendly green synthesis of a multifunctional silver nanocomposite (DS-MC-Ag-nanocomposite) utilizing ethanolic extract of waste date seeds ( Phoenix dactylifera ) and methyl cellulose (MC) as dual reducing and stabilizing agents. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Coumarins playing multiple roles in the life of plants also exhibit a wide range of positive effects for human health. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease (AD) represents a progressively growing worldwide public health burden. 3 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 →