27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Alzheimer's disease is a form of localized amyloidosis characterized by cerebral cortical amyloid plaques, neurofibrillary tangles, and amyloid deposits within the walls of leptomeningeal vessels. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cleavage of amyloid precursor protein (APP) by the beta- and gamma-secretases generates the amino and carboxy termini, respectively, of the A beta amyloidogenic peptides A beta40 and A beta42--the major constituents of the amyloid plaques in the brain parenchyma of Alzheimer's disease patients. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease is a leading cause of morbidity and mortality among the elderly. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Mutations in presenilin genes account for the majority of the cases of the familial form of Alzheimer's disease (FAD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Animal models of human diseases that accurately recapitulate clinical pathology are indispensable for understanding molecular mechanisms and advancing preclinical studies. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Presenilins are membrane proteins with multiple transmembrane domains that are thought to contribute to the development of Alzheimer's disease by affecting the processing of beta-amyloid precursor protein. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Linkage analysis was used to search the genome for chromosomal regions harboring familial Alzheimer's disease genes. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Approximately 10% of cases of Alzheimer's disease are familial and associated with autosomal dominant inheritance of mutations in genes encoding the amyloid precursor protein, presenilin 1 (PS1) and presenilin 2 (PS2). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Damage-associated microglia (DAM) profiles observed in Alzheimer's disease (AD)-related mouse models reflect an activation state that could modulate AD risk or progression. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Single-nucleus RNA sequencing (snRNA-seq) is used as an alternative to single-cell RNA-seq, as it allows transcriptomic profiling of frozen tissue. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Emerging evidence suggests that these morphological changes reflect functional alterations that affect disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Early expression disturbance of hub genes is an important feature of AD development, and interfering with this process may reverse the disease progression. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Recent research efforts provided compelling evidence of genome-wide DNA methylation alterations in aging and age-related disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is an age-associated neurodegenerative disease characterized by amyloidosis, tauopathy, and activation of microglia, the brain resident innate immune cells. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Progress toward the development of efficacious therapies for Alzheimer's disease (AD) is halted by a lack of understanding early underlying pathological mechanisms. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
In sprouting angiogenesis, specialized endothelial tip cells lead the outgrowth of blood-vessel sprouts towards gradients of vascular endothelial growth factor (VEGF)-A. VEGF-A is also essential for the induction of endothelial tip cells, but it is not known how single tip cells are selected to lead each vessel sprout, and how tip-cell numbers are determined. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Mutations in the PTEN-induced kinase 1 (PINK1) and Parkin RBR E3 ubiquitin-protein ligase (PARKIN) genes are associated with familial forms of Parkinson's disease (PD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Parkinson's disease (PD) is the second most common degenerative disorder. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most common form of dementia, an eversible, progressive disease that causes problems with memory, thinking, language, planning, and behavior. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid-related imaging abnormalities (ARIA), thought to reflect immune responses to vascular amyloid, have been detected in several amyloid-modifying therapy trials for Alzheimer's disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The past several decades have yielded deeper insights into the multifactorial pathogenesis and intervention strategies of Alzheimer's disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The lin-12 and glp-1 genes of Caenorhabditis elegans are members of the lin-12/Notch family of receptors for intercellular signals that specify cell fate. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
There appears to be a new syndrome in this family that is characterized by recurrent subcortical strokelike episodes, leukoencephalopathy, immunologic anomalies, muscular lipidosis, and an autosomal dominant pattern of transmission. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cockayne syndrome and xeroderma pigmentosum-Cockayne syndrome complex are rare autosomal recessive disorders with poorly understood biology. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Studies of diseases caused by mitochondrial DNA mutations suggest that a variety of degenerative processes may be associated with defects in oxidative phosphorylation (OXPHOS). 1 key finding →
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 →