Apolipoprotein E (APOE) is a lipid-transport protein abundantly expressed in most neurons in the central nervous system. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Apolipoprotein E (APOE) is a lipid-transport protein abundantly expressed in most neurons in the central nervous system. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is a progressive, neurodegenerative disease and the most common form of dementia in elderly people. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Hereditary frontotemporal dementia (FTD) is an autosomal dominant neurodegenerative disorder that is associated with mutations in the tau gene and with the pathological accumulation of hyperphosphorylated tau protein in affected brain cells in about a quarter of cases. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Review of clinical and biological features of primary progressive aphasia (PPA). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Deposits of amyloid fibers are found in large numbers in the walls of blood vessels and in neuritic plaques in the brains of patients with Alzheimer disease and adults with Down syndrome. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Genetic variation in the APOE gene and variation in chromosome 21 genotypes, including the APP locus, may influence age-associated cognitive decline in adults with Down syndrome. 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Parkinson's disease (PD) is a neurodegenerative disorder that is pathologically characterized by the presence of intracytoplasmic Lewy bodies, the major components of which are filaments consisting of alpha-synuclein. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Mutations in the human Cu,Zn superoxide dismutase gene (SOD1) are found in 20% of kindreds with familial amyotrophic lateral sclerosis. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Nosologically, Alzheimer disease is not a single disorder in spite of a common clinical phenotype. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Retinas of transgenic mice harboring a mutant presenilin (PS1) and a mutant APP gene were processed for TUNEL and immunohistochemistry with antibodies against APP, amyloid-beta, monocyte chemotactic protein (MCP)-1, and F4/80. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
MicroRNAs (miRNAs) are key regulatory RNAs known to repress mRNA translation through recognition of specific binding sites located mainly in their 3'-untranslated region (UTR). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Biochemical and genetic evidence establishes a central role of the amyloid precursor protein (APP) in Alzheimer disease (AD) pathogenesis. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Mutations in presenilins are responsible for approximately 40% of all early-onset familial Alzheimer disease (FAD) cases in which a genetic cause has been identified. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Since the discovery of the amyloid precursor protein (APP) in 1987, extensive research has been conducted analyzing the APP-derived beta-amyloid (Abeta) which is found in massive quantities in senile plaques of Alzheimer disease (AD) patients. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Alzheimer disease is the most common cause of dementia and represents a major public health problem. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Two common disorders of the elderly are heart failure and Alzheimer disease (AD). 4 key findings →
Participants: 315 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer disease (AD), the most common senile dementia, is characterized by amyloid plaques, vascular amyloid, neurofibrillary tangles, and progressive neurodegeneration. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
PSEN2 (presenilin 2) is one of the 3 proteins that, when mutated, causes early onset familial Alzheimer disease (FAD) cases. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We have recently shown acetylation of tau at lysine residue 280 (AC-K280) to be a disease-specific modification in Alzheimer disease (AD), corticobasal degeneration, and progressive supranuclear palsy, likely representing a major regulatory tau modification. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Processing of the amyloid precursor protein (APP) by γ-secretase results in generation of Aβ peptides of different lengths ranging from 51 to 30 residues. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Observations Genotype-phenotype correlations of AD are presented to provide a comprehensive appreciation of the spectrum of disease causation. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Accumulation of amyloid-β (Aβ), believed to be a key trigger of Alzheimer disease (AD), could result from impaired clearance mechanisms. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) genetics implies a causal role for innate immune genes, TREM2 and CD33, products that oppose each other in the downstream Syk tyrosine kinase pathway, activating microglial phagocytosis of amyloid (Aβ). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is a progressive neurodegenerative disorder and the most common form of dementia. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
This study aimed to investigate the effects of triggering receptor expressed on myeloid cell-2 (TREM2) on the production of pro-inflammatory mediators and cytokines induced by lipopolysaccharide (LPS) in BV2 microglia. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
10 of the 3,521 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 27,380 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 →