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Research

27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 1,001–1,025 of 1,346 studies (page 41 of 54) · 27,380 in the whole library · How the 0–100 score works

Showing 1,346 studies tagged precursor — clear

Browse by subject, author or institution

Each number is how many studies that link shows, with your other filters kept.

Subjects

Authors

Names as each record prints them; the same person can appear under two spellings.

Institutions

From OpenAlex; 12,859 studies have no institution on record and are not counted here.

A note on reading research. One study is rarely the final word.

We try to note the size of a study, whether it was in humans or animals, and how early-stage the finding is. If a summary here doesn't make that clear, treat it with extra caution and check the original source.

Apolipoprotein A-I deficiency increases cerebral amyloid angiopathy and cognitive deficits in APP/PS1DeltaE9 mice

✓ Peer-reviewed alzhub usefulness score 42 out of 100. The Journal of biological chemistry 2010-08-25

A hallmark of Alzheimer disease (AD) is the deposition of amyloid β (Aβ) in brain parenchyma and cerebral blood vessels, accompanied by cognitive decline. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Modulation of gene expression and cytoskeletal dynamics by the amyloid precursor protein intracellular domain (AICD)

✓ Peer-reviewed alzhub usefulness score 42 out of 100. Molecular biology of the cell 2006-11-08

Amyloidogenic processing of the amyloid precursor protein (APP) results in the generation of beta-amyloid, the main constituent of Alzheimer plaques, and the APP intracellular domain (AICD). 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Characterization of alpha 2,6-sialyltransferase cleavage by Alzheimer's beta -secretase (BACE1)

✓ Peer-reviewed alzhub usefulness score 42 out of 100. The Journal of biological chemistry 2002-12-07

BACE1 is a membrane-bound aspartic protease that cleaves the amyloid precursor protein (APP) at the beta-secretase site, a critical step in the Alzheimer disease pathogenesis. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Generation and regulation of beta-amyloid peptide variants by neurons

✓ Peer-reviewed alzhub usefulness score 42 out of 100. Journal of neurochemistry 1998-11-01

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

Deposition of beta/A4 immunoreactivity and neuronal pathology in transgenic mice expressing the carboxyl-terminal fragment of the Alzheimer amyloid precursor in the brain

✓ Peer-reviewed alzhub usefulness score 42 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1992-11-01

The deposition of amyloid in senile plaques and along the walls of the cerebral vasculature is a characteristic feature of Alzheimer disease. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Microbiome-generated amyloid and potential impact on amyloidogenesis in Alzheimer's disease (AD)

✓ Peer-reviewed alzhub usefulness score 42 out of 100. Journal of nature and science 2015-07-01

According to the ' amyloid cascade hypothesis of Alzheimer's disease ' first proposed about 16 years ago, the accumulation of Aβ peptides in the human central nervous system (CNS) is the primary influence driving Alzheimer's disease (AD) pathogenesis, and Aβ peptide accretion is the result of an imbalance between Aβ peptide production and clearance. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Onset of Alzheimer disease in apolipoprotein ɛ4 carriers is earlier in butyrylcholinesterase K variant carriers

✓ Peer-reviewed alzhub usefulness score 42 out of 100. BMC neurology 2024-04-09

The authors sought to examine the impact of the K-variant of butyrylcholinesterase (BCHE-K) carrier status on age-at-diagnosis of Alzheimer disease (AD) in APOE4 carriers. 4 key findings →

Design: post-hoc analysis Participants: 33 Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Increased monoamine oxidase B activity in plaque-associated astrocytes of Alzheimer brains revealed by quantitative enzyme radioautography

✓ Peer-reviewed alzhub usefulness score 42 out of 100. Neuroscience 1994-09-01

The aetiology and pathogenesis of Alzheimer's disease are currently poorly understood, but symptomatic disease is associated with amyloid plaques, neurofibrillary tangles, neuronal loss and numerous alterations of neurotransmitter systems in the CNS. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Full text may need a subscription

Evidence that aging and amyloid promote microglial cell senescence

✓ Peer-reviewed alzhub usefulness score 42 out of 100. Rejuvenation research 2007-03-01

Advanced age and presence of intracerebral amyloid deposits are known to be major risk factors for development of neurodegeneration in Alzheimer's disease (AD), and both have been associated with microglial activation. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Full text may need a subscription

The role of activated astrocytes and of the neurotrophic cytokine S100B in the pathogenesis of Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 42 out of 100. Neurobiology of aging 2001-11-01

Activated astrocytes, overexpressing the neurotrophic signaling molecule S100beta, are invariant components of the Abeta plaques of Alzheimer's disease. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Full text may need a subscription

Sex Differences in Neuropathology and Cognitive Behavior in APP/PS1/tau Triple-Transgenic Mouse Model of Alzheimer's Disease

✓ Peer-reviewed alzhub usefulness score 42 out of 100. Neuroscience bulletin 2018-08-11

Alzheimer's disease (AD) is the most common form of dementia among the elderly, characterized by amyloid plaques, neurofibrillary tangles, and neuroinflammation in the brain, as well as impaired cognitive behaviors. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

APOE‐Genotype Modifies the Association of Meat Consumption with Cognitive Decline: Longitudinal Analyses of The Swedish National Study on Aging and Care, SNAC‐K

✓ Peer-reviewed alzhub usefulness score 42 out of 100. Alzheimer s & Dementia 2025-12-01

Higher total meat consumption (red meat: 51%, poultry: 20%, processed meat: 29%), was associated with a better cognitive trajectory only in the APOE34/44 stratum (β per 1 z-unit increase: 0.011; CI: 0.004 to 0.018 versus -0.003; CI: -0.008 to 0.003; P for interaction = 0.002). 5 key findings →

Design: longitudinal study Evidence: moderate

Full summary, score breakdown and related studies → Original source Free full text

Brain delivery of a neurotrophic peptide derived from secreted amyloid precursor protein APPsα as a therapeutic strategy for Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 42 out of 100. Journal of Controlled Release 2025-11-02

Whereas neurotoxic Aβ is derived from amyloid precursor protein (APP) by β- and γ-secretase cleavage, APP processing along the non-amyloidogenic pathway results in the secretion of the large neurotrophic ectodomain APPsα. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

The ER protein CANX (calnexin)-mediated autophagy protects against alzheimer disease

✓ Peer-reviewed alzhub usefulness score 42 out of 100. Autophagy 2025-01-15

Although the relationship between macroautophagy/autophagy and Alzheimer disease (AD) is widely studied, the underlying mechanisms are poorly understood, especially the regulatory role of the initiation signaling of autophagy on AD. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Presenilin-1 Familial Alzheimer Mutations Impair γ-Secretase Cleavage of APP Through Stabilized Enzyme–Substrate Complex Formation

✓ Peer-reviewed alzhub usefulness score 42 out of 100. Biomolecules 2025-07-01

Familial Alzheimer's disease (FAD) is caused by dominant missense mutations in amyloid precursor protein (APP) and presenilin-1 (PSEN1), the catalytic component of γ-secretase that generates amyloid β-peptides (Aβ) from the APP C-terminal fragment C99. 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

S100 beta protein expression in Alzheimer disease: potential role in the pathogenesis of neuritic plaques

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Journal of neuroscience research 1994-11-01

Increased synthesis and release of S100 beta protein from activated astrocytes has been implicated in the overgrowth of dystrophic neurites in neuritic plaques in Alzheimer disease (AD). 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Full text may need a subscription

Glutamatergic alterations and mitochondrial impairment in a murine model of Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Neurobiology of aging 2011-10-27

Deficits in glutamate neurotransmission and mitochondrial functions were detected in the frontal cortex (FC) and hippopcampus (HIPP) of aged 3×Tg-Alzheimer's disease (AD) mice, compared with their wild type littermates (non-Tg). 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Full text may need a subscription

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.

↑ Change the filters

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 27,380 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.

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 27,380 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 →

Newest studies, as a dated timeline →    Atom feed