29,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
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
Full summary, score breakdown and related studies → Original source Free full text
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
This method differentiated eight tauopathies, including Alzheimer's disease, Pick disease, progressive supranuclear palsy (PSP), corticobasal degeneration (CBD), argyrophilic grain disease (AGD), frontotemporal dementia with parkinsonism associated with chromosome 17 with N279K mutation (FTDP-17 N279K), and globular glial tauopathies types II and III. 5 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
Changes in the metabolic activity within the brain of patients suffering from Alzheimer's disease (AD) were investigated and compared with biochemical alterations in the hippocampus induced by fimbria/fornix transection in the rat. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Alzheimer type II astrocytosis is the pathological hallmark of hepatic encephalopathy. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
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
Full summary, score breakdown and related studies → Original source Full text may need a subscription
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
Full summary, score breakdown and related studies → Original source Full text may need a subscription
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
Oxidative stress in DS is associated with neurodevelopmental defects, neuronal dysfunction, and the onset of dementia re-sembling Alzheimer's disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Of note, using large-scale transcriptome and chromatin profiling, we show that T cell shape microglia-specific metabolic plasticity in both genetic and epigenetic resolution. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Monoclonal antibodies such as lecanemab and donanemab show reduction in amyloid plaque and slowing of cognitive and functional decline (modest) in early AD (mild cognitive impairment or mild dementia). 5 key findings →
Design: narrative review Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Monoclonal antibodies such as lecanemab and donanemab show reduction in amyloid plaque and slowing of cognitive and functional decline (modest) in early AD (mild cognitive impairment or mild dementia). 5 key findings →
Design: narrative review Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer’s disease (AD) is characterized by progressive accumulation of amyloid-β (Aβ) peptides, initiating a pathological cascade from soluble monomers to toxic oligomers, protofibrils, fibrils, and ultimately extracellular amyloid plaques that contribute to synaptic dysfunction and neuronal degeneration. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Dementia is a progressive neurodegenerative disorder that represents a growing challenge to global health, especially in aging populations. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Our study is the first one showing that dietary supplements improve cognition and sleep in a mouse model of DS. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
CWPs consist predominantly of two novel arrangements of type I Aβ filaments, and we have designated them as type Ic and type Id Aβ filaments. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We identified an interaction between TDP-43 and APOE through immunoprecipitation followed by proteomics in mice, verified in human brain by co- immunoprecipitation. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Primary cortical neurons with C9orf72 haploinsufficiency exhibit alterations in dendritic branching, indicating disrupted neuronal connectivity. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
10 of the 8,203 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 29,780 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 29,780 records, built mostly from automated pulls of Europe PMC (63.8% of the library) and OpenAlex (17.1%), 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.
1,037 records (3.5% of the library) are not peer-reviewed — 964 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 →