27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Growing genetic and pathological evidence has identified microglial dysfunction as a key contributor to the pathogenesis and progression of various neurological disorders, positioning microglia replacement as a promising therapeutic strategy. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Triggering receptor expressed on myeloid cells 2 (TREM2) dysfunction contributes to Alzheimer's disease pathogenesis, yet current therapeutics cannot prevent ADAM-mediated receptor shedding that diminishes signaling efficacy. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Microglia play a pivotal role in the pathology of Alzheimer's Disease (AD), with the Triggering Receptor Expressed on Myeloid cells 2 (TREM2) central to their neuroprotective functions. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neuroinflammation driven by microglial activation is a hallmark of Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
ITM2B/BRI2 mutations cause Alzheimer's Disease (AD)-related dementias. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
TREM2, a microglia-specific receptor, is strongly associated with Alzheimer's disease (AD) risk, mediating microglial responses to amyloid pathology critical to AD development. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neurodegenerative diseases, including Alzheimer's disease (AD), Parkinson's disease (PD), and amyotrophic lateral sclerosis (ALS), represent significant global health challenges, affecting millions and straining healthcare systems. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Triggering receptor expressed on myeloid cells 2 (TREM2) is a membrane glycoprotein that plays a crucial role in the regulation of microglial survival, activation, phagocytosis, as well as in the maintenance of brain homeostasis and the inflammatory response to injury or neurodegeneration. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Our results showed that IHT ameliorated cognitive function and Aβ pathology. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We proved their efficacy in human iPSC microglia in vitro, as well as their pharmacological activity in vivo in a xenografted microglia model. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Causative mutations in the genes encoding amyloid precursor protein (APP), presenilin 1 (PSEN1), or presenilin 2 (PSEN2) account for a majority of cases of familial Alzheimer disease (FAD) inherited in an autosomal-dominant pattern. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a complex neurodegenerative disorder influenced by various genetic factors. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We identified common disease endotypes, such as dedifferentiation, dysregulation of synaptic signaling, repression of mitochondrial function and metabolism, and inflammation. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a complex neurodegenerative disorder and the most common form of dementia. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Autosomal dominant Alzheimer's disease (ADAD) is driven by rare variants in APP, PSEN1, and PSEN2. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease is a progressive neurodegenerative disorder and the most common cause of dementia that principally affects older adults. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Circular RNAs (circRNAs) are emerging as a promising object of study in Alzheimer's disease (AD) pathogenesis. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Mutations in the PSEN genes are the major cause of familial Alzheimer's disease, and presenilin (PS) is the catalytic subunit of γ-secretase, which cleaves type I transmembrane proteins, including the amyloid precursor protein (APP) to release Aβ peptides. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Somatic mutations are DNA sequence changes that occur in non-reproductive cells during an organism's life and are not inherited by offspring. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Mutations in PSEN1 are the most common cause of autosomal dominant familial Alzheimer's disease (FAD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Dementia is a syndrome that can cause a number of progressive illnesses that affect memory, thinking, and ability to perform everyday tasks. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Parkinson's disease (PD) is a prevalent neurodegenerative disorder, and recent evidence suggests that pathogenesis may be in part mediated by inflammatory processes, the molecular and cellular architectures of which are largely unknown. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebrovascular dysfunction underlies many neurological disorders, yet how genetic variants in brain vascular cells drive disease risk remains unknown. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Highly penetrant autosomal dominant Alzheimer's disease (ADAD) comprises a distinct disease entity as compared to the far more prevalent form of AD in which common variants collectively contribute to risk. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The study of transcriptomic and epigenomic variations in neurodegenerative diseases, particularly tauopathies like Pick's disease (PiD) and Alzheimer's disease (AD), offers insights into their underlying regulatory mechanisms. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
10 of the 3,549 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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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 →