28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Vascular dementia (VaD) is recognized as the second most prevalent form of dementia after Alzheimer's disease, with its pathogenesis intricately associated with cerebrovascular pathologies, including chronic hypoperfusion, oxidative stress, and neuroinflammation. 2 key findings →
Design: narrative review Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
MDVs are small vesicles that bud from mitochondria and play an important role in removing damaged mitochondrial components. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Microglia are central regulators of Alzheimer's disease pathogenesis, but their roles cannot be reduced to a simple protective-versus-harmful dichotomy. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In 2004, the first radiotracer that bound amyloid plaques was reported, which enabled visualization of the amount and regional distribution of amyloid plaques in the brains of living individuals via positron emission tomography (PET). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Cystatin C (CST3) colocalizes with amyloid-β (Aβ) around vessels in cerebral amyloid angiopathy (CAA). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Since the term limbic-predominant age-related TDP-43 encephalopathy (LATE) was coined in 2019, more than 200 articles addressing the subject were published. 1 key finding →
Evidence: low
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As the term limbic-predominant age-related transactive response DNA-binding protein 43 (TDP-43) encephalopathy (LATE) was coined in 2019, more than 200 articles addressing the subject were published. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
This review explores the complex relationship between neuroinflammation and cognitive decline in individuals with Type 2 Diabetes (T2D). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
According to the latest report in 2024 by the World Health Organization, based on global data from 2021, Alzheimer’s disease (AD) and other forms of dementia rank seventh among the leading causes of death worldwide, with an estimated 1.8 million deaths. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Acupuncture ameliorated cognitive impairment in VD rats, reduced hippocampal neuronal damage and apoptosis, downregulated pro-apoptotic proteins (cleaved-caspase 3 and Bax), and upregulated anti-apoptotic Bcl-2. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We recently confirmed and extended these findings using recombinant TauOs generated from full-length human tau in the presence of arachidonic acid (Balducci et al., 2025; Figure 1). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
2′-FL improved cognitive performance in 5xFAD mice, reduced Aβ plaque deposition and pro-inflammatory cytokine levels in vivo , and mitigated oxidative stress and synaptic dysfunction in cellular models. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The locus of the gene PTK2B encoding the tyrosine kinase Pyk2 has been associated with the risk of late-onset Alzheimer’s disease, the predominant form of dementia. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Semantic dementia (SD) is a type of dementia characterized by a loss of semantic memory, typically presenting with left-predominant temporal lobe atrophy and a frontotemporal lobar degeneration with TDP-43 (FTLD-TDP) type C pathology. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In AβO-injected mice, AR, particularly at 200 mg/kg, attenuated memory deficits, reduced hippocampal neuronal degeneration, preserved synaptic protein immunoreactivity and increased markers of hippocampal cell proliferation and immature neurons. 5 key findings →
Evidence: low
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Beyond their role in energy production, mitochondria also interact with other organelles through forming membrane contacts that serve as central hubs of cellular metabolism and signaling. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Defective mitochondrial quality control is increasingly implicated in tau-mediated neurodegeneration, but how distinct tau lesions in different cell types interact with PINK1-PRKN-mediated mitophagy remains unclear. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's Disease (AD) remains a significant global health challenge, characterized by progressive neurodegeneration and a decline in cognitive abilities such as memory and learning. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
This study offers evidence of functional and neuroprotective effects of two weeks treatment with a Ptychopetalum olacoides extract against Aβ peptide-induced neurotoxicity in mice. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Transmissible encephalopathies (TSEs), such as Creutzfeldt-Jakob disease (CJD) and scrapie, are caused by infectious agents that provoke strain-specific patterns of disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The 5' untranslated region (UTR) of the APP gene, encompassing 147 base pairs between the transcriptional (+1) and the translational start site, was examined for its role in APP expression. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Researchers since the 1990s have predominantly focused on the amyloid hypothesis and the formation of amyloid fibrils as the culprit behind AD when we began working on soluble Abeta (sAbeta). 2 key findings →
Evidence: low
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Paired helical filaments (PHF), which constitute neurofibrillary tangles (NFT) and neuritic plaque (NP) neurites, serve as a useful marker for Alzheimer disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The occurrence of +1 frameshifted proteins, such as amyloid precursor protein (APP+1) and ubiquitin-B (UBB+1) in Down syndrome (DS) has been linked to the onset of Alzheimer's disease (AD). 1 key finding →
Evidence: low
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Down syndrome (DS), caused by trisomy of chromosome 21, is characterized by early-onset oxidative stress, impaired neuronal development, and an increased risk of Alzheimer's disease (AD)-like neuropathology. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
10 of the 6,890 studies in this tag, 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 28,180 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 →