Amyloid deposition is a neuropathological hallmark of Alzheimer's disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Research
27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Interleukin-1 (IL-1), an inflammatory cytokine overexpressed in the neuritic plaques of Alzheimer's disease, activates astrocytes and enhances production and processing of beta-amyloid precursor protein (beta-APP). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Immunization with preaggregated amyloid beta-peptide (Abeta(1-42)) and administration of antibodies against Abeta into amyloid precursor protein APP(V717F)- transgenic mice (an animal model of AD) have recently been reported to dramatically reduce amyloid plaque deposition, neuritic dystrophy, and astrogliosis, most likely by enhancing Abeta clearance from brain. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
FE65 binds to the Alzheimer amyloid precursor protein (APP), but the function of this interaction has not been identified. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Amyloid precursor protein (APP) metabolism is central to the pathogenesis of Alzheimer disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Iron influx increases the translation of the Alzheimer amyloid precursor protein (APP) via an iron-responsive element (IRE) RNA stem loop in its 5'-untranslated region. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Vaccination against human beta-amyloid peptide (A beta) has been shown to remove the amyloid burden produced in transgenic mice overexpressing the mutated human amyloid precursor protein (APP) gene. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
We review the clinical, radiologic, and neuropathologic features of the hereditary and sporadic forms of cerebral amyloid angiopathy (CAA) associated with vascular deposition of the beta-amyloid peptide. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
High serum/plasma cholesterol levels have been suggested as a risk factor for Alzheimer's disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Numerous studies have demonstrated oxidative damage in the central nervous system in subjects with Alzheimer disease and in animal models of this dementing disorder. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Proteolysis of the amyloid precursor protein (APP) liberates various fragments including the proposed initiator of Alzheimer disease-associated dysfunctions, amyloid-β. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer disease amyloid beta-peptide (Abeta) is generated via proteolytic processing of the beta-amyloid precursor protein by beta- and gamma-secretase. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Trafficking and proteolytic processing of amyloid precursor protein (APP) have been the focus of numerous investigations in the past two decades, since the identification of Abeta as the principal component of brain senile plaques and the cloning of APP cDNA. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
47/100
The proteolytic processing of amyloid precursor protein (APP) to generate the neurotoxic amyloid β (Aβ) peptide is central to the pathogenesis of Alzheimer disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Clinical differential diagnosis of early-onset dementia (EOD) includes familial Alzheimer disease (FAD) and hereditary prion disease. 4 key findings →
Participants: 16 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Recent evidence suggests that statin use may be associated with a decreased risk for Alzheimer disease, although the mechanisms underlying this apparent risk reduction are poorly understood. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Calbindin-D28k (CB), one of the major calcium-binding and buffering proteins, has a critical role in preventing a neuronal death as well as maintaining calcium homeostasis. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We hypothesized that de novo variants (DNV) might participate in the genetic determinism of sporadic early-onset Alzheimer disease (EOAD, onset before 65 years). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Alzheimer's disease (AD) is an irreversible, devastating neurodegenerative brain disorder characterized by the loss of neurons and subsequent cognitive decline. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In the past five years, a series of large-scale genetic studies have revealed novel risk factors for Alzheimer's disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
47/100
One of the largest unmet medical needs is a disease-modifying treatment for Alzheimer's disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
47/100
Microglia affect Alzheimer's disease (AD) pathogenesis in opposing manners, by protecting against amyloid accumulation in early phases of the disease and promoting neuropathology in advanced stages. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Microglia-specific genetic variants are enriched in several neurodegenerative diseases, including Alzheimer's disease (AD), implicating a central role for alterations of the innate immune system in the disease etiology. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is an incurable neurodegenerative disease currently affecting 1.75% of the US population, with projected growth to 3.46% by 2050. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Mechanisms underlying the protective effect of apolipoprotein E ( APOE ) ε2 against Alzheimer’s disease (AD) are not well understood. 4 key findings →
Participants: 982 Evidence: low
Full summary, score breakdown and related studies → Original source
From across this tag
10 of the 1,344 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.
- A biophysical and molecular characterization of the interaction between the Alzheimer risk factor BIN1 and the neuronal scaffold protein p140Cap
- Alzheimer disease Abeta production in the absence of S-palmitoylation-dependent targeting of BACE1 to lipid rafts
- Longitudinally persisting KCNA2-autoantibodies in mild amnestic dementia with Alzheimer´s pathology - Report and literature review
- Upregulated function of mitochondria-associated ER membranes in Alzheimer disease
- β-Amyloid impairs axonal BDNF retrograde trafficking
- Oxygen extraction fraction is differentially associated with pathological biomarkers in Alzheimer’s disease and non-Alzheimer’s dementias
- Profiling characteristics of plasma exosomal miRNAs across cognitive stages: from normalcy to mild cognitive impairment and Alzheimer's disease
- Analysis of European mitochondrial haplogroups with Alzheimer disease risk
- A plasma protein signature for cerebral amyloid angiopathy
- Impaired insulin secretion increases the risk of Alzheimer disease
Where “Free full text” comes from
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
How the 0–100 score works — and why some entries are capped
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.
- Journal tier up to 10 pts
- Journal's citation record up to 4 pts
- Study design up to 12 pts
- Strength of evidence up to 5 pts
- Peer-review validation up to 10 pts
- How recent up to 5 pts
- Sample size up to 4 pts
- Effect reported up to 3 pts
- Studied in people up to 3 pts
- Randomised / blinded up to 2 pts
- Times cited up to 7 pts
- Citations per year up to 5 pts
- Impact for its field and year up to 6 pts
- Cited by studies here up to 6 pts
- Still being cited up to 4 pts
- Senior author's track record up to 4 pts
- Institution's track record up to 3 pts
- Multi-centre collaboration up to 3 pts
- Indexed in PubMed up to 2 pts
- Free to read up to 2 pts
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.
What this library is — and isn't
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 →