These findings lay groundwork to enable AD clinical trials with characterization and disease-specific tracking of DS adults. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
31,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
These findings lay groundwork to enable AD clinical trials with characterization and disease-specific tracking of DS adults. 3 key findings →
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
APP expression misregulation can cause genetic Alzheimer's disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Older patients with kidney failure residing in high-disadvantage neighborhoods, particularly Black patients and those in suburban, rural, or small-town areas, had a higher risk of ADRD compared with those in low-disadvantage neighborhoods. 5 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
MCI prevalence was comparable across groups (7.5%-8.0%), but progression to dementia varied (9.4% Black vs. 11.4% Other). 5 key findings →
Participants: 83,180 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Fourteen individuals with DS and five age-matched euploid controls were studied, with all DS cases showing HFOs. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The neuronal lysosomal system is a major degradative pathway, induced by cell stress and closely linked to Alzheimer disease (AD) and other neurodegenerative diseases. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
NHB Hispanic, and NHW participants prevalences were APOE ε4 (32.2%, 27.4%, 17.6%), diabetes (26.1%, 35.0%, 13.9%), hypertension (79.0%, 63.6%, 58.2%), obesity (56.8%, 50.3%, 38.5%), and tobacco dependence (12.9%, 7.5%, 3.9%). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
More than 50% of older adults with AD/ADRD visit the emergency department (ED) each year [3, 4] and those who do are seriously ill, have significant healthcare costs (e.g., hospital admissions, repeat ED visits) and mortality [4-6]. 5 key findings →
Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Accumulation of β-amyloid (Aβ) in the brain is a key event in Alzheimer disease pathogenesis. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
β-amyloid precursor protein (APP) and amyloid beta peptide (Aβ) are strongly implicated in Alzheimer's disease (AD) pathogenesis, although recent evidence has linked APP-βCTF generated by BACE1 (β-APP cleaving enzyme 1) to the development of endocytic abnormalities and cholinergic neurodegeneration in early AD. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Triplication of chromosome 21 in Down syndrome (DS) results in overexpression of the minibrain kinase/dual-specificity tyrosine phosphorylated and regulated kinase 1A gene (DYRK1A). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The findings of this study are consistent with previous reports demonstrating a high aggregation propensity of Aβ 4-x peptides and suggest an important role of these N-truncated Aβ species in the process of amyloidogenesis and plaque core formation. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Fifty-three scans (31.74%) were rated amyloid-positive by all readers, while 62 scans (37.13%) were rated as amyloid-negative by all readers. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The rising prevalence of Alzheimer's disease and Alzheimer's disease–related dementias has led to renewed public discourse and policy changes in response to the care needs of persons living with dementia and their care partners. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
These findings identify affiliate stigma as an important risk factor for dementia caregivers’ depressive symptoms, operating through both objective and emotional forms of social disconnection. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The overall rate of dementia was higher in PLHIV than that in POHIV (22% vs 10%; p = 1.4e). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Familial Danish dementia is an early onset autosomal dominant neurodegenerative disorder linked to a genetic defect in the BRI2 gene and clinically characterized by dementia and ataxia. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
A population of >6 million people worldwide at high risk of Alzheimer’s disease (AD) are those with Down Syndrome (DS, caused by trisomy 21 (T21)), 70% of whom develop dementia during lifetime, caused by an extra copy of β-amyloid-(Aβ)-precursor-protein gene. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Studies of processing of the Alzheimer beta-amyloid precursor protein (betaAPP) have been performed to date mostly in continuous cell lines and indicate the existence of two principal metabolic pathways: the "beta-secretase" pathway, which generates beta-amyloid (A beta(1-40/42); approximately 4 kDa), and the "alpha-secretase" pathway, which generates a smaller fragment, the "p3" peptide (A beta(17-40/42); approximately 3 kDa). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The clinical impact of Alzheimer's disease pathology at biopsy was investigated in 56 cognitively impaired patients undergoing shunt surgery for idiopathic normal pressure hydrocephalus (NPH). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Worldwide, over half of all individuals with dementia are undiagnosed. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In this sample of older individuals, a higher dropout rate occurred in those assigned to the high-technology assessment techniques; however, once participants had completed baseline in all 3 arms, they continued participation through 1 month. 2 key findings →
Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is the most common cause of dementia worldwide. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Endocytic system dysfunction is one of the earliest disturbances that occur in Alzheimer's disease (AD), and may underlie the selective vulnerability of cholinergic basal forebrain (CBF) neurons during the progression of dementia. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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.
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 31,780 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 31,780 records, built mostly from automated pulls of Europe PMC (66% of the library) and OpenAlex (16%), 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.
1,052 records (3.3% of the library) are not peer-reviewed — 973 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 →
Newest studies, as a dated timeline → Atom feed Where this research is being discussed: events