The cause of Alzheimer's disease (AD) is unknown. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
The cause of Alzheimer's disease (AD) is unknown. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Recent studies have suggested that neuronal death in Alzheimer's disease or ischemia could arise from dysfunction of the endoplasmic reticulum (ER). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
ABCA1 is an ATP-binding cassette protein that transports cellular cholesterol and phospholipids onto high density lipoproteins (HDL) in plasma. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Presenilins (PSs) are required for Notch signaling in the development of vertebrates and invertebrates. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Aggregation and cytotoxicity of misfolded alpha-synuclein is postulated to be crucial in the disease process of neurodegenerative disorders such as Parkinson's disease and DLB (dementia with Lewy bodies). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Multiple lines of evidence implicate beta-amyloid (Abeta) in the pathogenesis of Alzheimer's disease (AD), but the mechanisms whereby Abeta is involved remain unclear. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Beta-amyloid (betaA) peptide is strongly implicated in the neurodegeneration underlying Alzheimer's disease, but the mechanisms of neurotoxicity remain controversial. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Disruption of axonal transport leads to a disorganized distribution of mitochondria and other organelles and is thought to be responsible for some types of neuronal disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Dementia is a frequent complication of Parkinson's disease (PD) and usually occurs late in the protracted course of the illness. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Collagenous Alzheimer amyloid plaque component (CLAC) is a unique non-Abeta amyloid component of senile plaques (SP) derived from a transmembrane collagen termed CLAC-precursor. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Early diagnosis of Alzheimer s disease (AD) is relevant in order to initiate symptomatic treatment with antidementia drugs. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Disability, characterised by the loss of ability to perform activities of daily living (ADL), is a defining feature of dementia that results in growing caregiver burden and the eventual need for alternative care or nursing home placement. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
There is a well-documented tendency for cognitive tests to underestimate the abilities of older people in black and minority ethnic groups. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
It has been clearly established that there is an increased incidence of early onset dementia of the Alzheimer type (DAT) in people who have Down syndrome. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
The binding of amyloid beta peptides (Abeta) to plasma membranes appears to be a promising point of intervention in the events leading to the development of Alzheimer's disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Increasing evidence indicates that there are reductions in estrogen and androgen levels in aged men and women. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Apolipoprotein E (ApoE) is the major lipid-carrier protein in the brain, and several studies provided evidence that ApoE epsilon4 allele can be considered a genetic risk factor for vascular diseases. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Chronically activated glia associated with amyloid plaques might contribute to neuronal dysfunction in Alzheimer's disease (AD) through generation of neuroinflammatory molecules. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The noninvasive techniques of static and dynamic light scattering are emerging as valuable diagnostic tools for the early detection of ocular and systemic diseases. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebrovascular disease (CVD), as well as secondary ischemic brain injury from cardiovascular disease, are common causes of dementia and cognitive decline in the elderly. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The management of dementia in Alzheimer's disease has dramatically changed since the development of anti-dementia drugs. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
HIV-associated dementia (HAD) is a complication of advanced HIV disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
When diagnosis of dementia occurs earlier in the disease process, more time is available for treatment aimed at maintaining patient function and delaying decline, and for family education about the disease and its management. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Neurodegeneration in fetal development of Down syndrome (DS) patients is proposed to result in apparent neuropathological abnormalities and to contribute to the phenotypic characteristics of mental retardation and premature development of Alzheimer disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
The molecular mechanisms of beta-amyloidogenesis in sporadic Alzheimer's disease are still poorly understood. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
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 →