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Research

27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 826–850 of 1,346 studies (page 34 of 54) · 27,780 in the whole library · How the 0–100 score works

Download bibliography of the first 500 of these studies, in this order: BibTeX (.bib) · RIS (.ris)

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; 13,259 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.

Inflammatory processes induce beta-amyloid precursor protein changes in mouse brain

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1995-03-01

In Alzheimer disease, a combination of genetic predisposition and environmental factors may contribute to changes in beta-amyloid precursor protein (APP) expression, beta-amyloid peptide deposition, and neuronal loss. 4 key findings →

Evidence: low

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

Lysosomal proteinase antigens are prominently localized within senile plaques of Alzheimer's disease: evidence for a neuronal origin

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Brain research 1990-04-01

To investigate the role of proteolysis in amyloid formation, we studied the localization of the proteolytic enzymes, cathepsin D and cathepsin B, in the prefrontal cerebral cortex and hippocampus of human postmortem brains from patients with Alzheimer's disease and from individuals free of neurological disease. 4 key findings →

Evidence: low

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

Muscarinic regulation of Alzheimer's disease amyloid precursor protein secretion and amyloid beta-protein production in human neuronal NT2N cells

✓ Peer-reviewed alzhub usefulness score 45 out of 100. The Journal of biological chemistry 1995-03-01

The Alzheimer amyloid precursor protein (APP) undergoes complex processing resulting in the production of a 4-kDa amyloid peptide (A beta) which has been implicated in the pathogenesis of Alzheimer's disease. 4 key findings →

Evidence: low

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

The familial dementia BRI2 gene binds the Alzheimer gene amyloid-beta precursor protein and inhibits amyloid-beta production

✓ Peer-reviewed alzhub usefulness score 45 out of 100. The Journal of biological chemistry 2005-06-27

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

Regulated formation of Golgi secretory vesicles containing Alzheimer beta-amyloid precursor protein

✓ Peer-reviewed alzhub usefulness score 45 out of 100. The Journal of biological chemistry 1995-10-01

Phorbol esters, activators of protein kinase C (PKC), regulate the relative utilization of alternative processing pathways for the Alzheimer beta-amyloid precursor protein (beta-APP) in intact cells, increasing the production of nonamyloidogenic soluble beta-APP (s beta-APP) and decreasing that of neurotoxic beta-amyloid (A beta) peptide. 3 key findings →

Evidence: low

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

Brain oligomeric β-amyloid but not total amyloid plaque burden correlates with neuronal loss and astrocyte inflammatory response in amyloid precursor protein/tau transgenic mice

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Journal of neuropathology and experimental neurology 2011-05-01

It has long been assumed that β-amyloid (Aβ) had to assemble into fibrillar amyloid plaques to exert its neurotoxic effects in Alzheimer disease. 4 key findings →

Evidence: low

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

Exercise is more effective than diet control in preventing high fat diet-induced β-amyloid deposition and memory deficit in amyloid precursor protein transgenic mice

✓ Peer-reviewed alzhub usefulness score 45 out of 100. The Journal of biological chemistry 2012-05-04

Accumulating evidence suggests that some dietary patterns, specifically high fat diet (HFD), increase the risk of developing sporadic Alzheimer disease (AD). 4 key findings →

Evidence: low

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

Characterization of intermediate steps in amyloid beta (Aβ) production under near-native conditions

✓ Peer-reviewed alzhub usefulness score 45 out of 100. The Journal of biological chemistry 2013-11-13

Processing of the amyloid precursor protein (APP) by γ-secretase results in generation of Aβ peptides of different lengths ranging from 51 to 30 residues. 4 key findings →

Evidence: low

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

Increased expression of beta-amyloid precursor protein during neuronal differentiation is not accompanied by secretory cleavage

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1992-10-01

Despite increasing evidence for a pathogenetic role for the beta-amyloid precursor protein (beta APP) in Alzheimer disease, the physiological function of the protein remains unclear. 4 key findings →

Evidence: low

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

Rodent A beta modulates the solubility and distribution of amyloid deposits in transgenic mice

✓ Peer-reviewed alzhub usefulness score 45 out of 100. The Journal of biological chemistry 2007-06-07

The amino acid sequence of amyloid precursor protein (APP) is highly conserved, and age-related A beta aggregates have been described in a variety of vertebrate animals, with the notable exception of mice and rats. 4 key findings →

Evidence: low

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

Curcumin restores innate immune Alzheimer's disease risk gene expression to ameliorate Alzheimer pathogenesis

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Neurobiology of disease 2019-04-02

Alzheimer's disease (AD) genetics implies a causal role for innate immune genes, TREM2 and CD33, products that oppose each other in the downstream Syk tyrosine kinase pathway, activating microglial phagocytosis of amyloid (Aβ). 4 key findings →

Evidence: low

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

Amyloid Precursor Protein (APP) Metabolites APP Intracellular Fragment (AICD), Aβ42, and Tau in Nuclear Roles

✓ Peer-reviewed alzhub usefulness score 45 out of 100. The Journal of biological chemistry 2015-08-21

Amyloid precursor protein (APP) metabolites (amyloid-β (Aβ) peptides) and Tau are the main components of senile plaques and neurofibrillary tangles, the two histopathological hallmarks of Alzheimer disease. 3 key findings →

Evidence: low

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

Key Aging-Associated Alterations in Primary Microglia Response to Beta-Amyloid Stimulation

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Frontiers in aging neuroscience 2017-08-31

Alzheimer's disease (AD) is characterized by a progressive cognitive decline and believed to be driven by the self-aggregation of amyloid-β (Aβ) peptide into oligomers and fibrils that accumulate as senile plaques. 4 key findings →

Evidence: low

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

Replacement of brain-resident myeloid cells does not alter cerebral amyloid-β deposition in mouse models of Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 45 out of 100. The Journal of experimental medicine 2015-10-12

Immune cells of myeloid lineage are encountered in the Alzheimer's disease (AD) brain, where they cluster around amyloid-β plaques. 4 key findings →

Evidence: low

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

INPP5D deficiency attenuates amyloid pathology in a mouse model of Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Alzheimer's & dementia : the journal of the Alzheimer's Association 2022-12-16

A non-coding variant (rs35349669) in INPP5D increases the risk for Alzheimer's disease (AD), and elevated INPP5D expression is associated with increased plaque deposition. 4 key findings →

Evidence: low

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

Dephosphorylation of Alzheimer paired helical filaments by protein phosphatase-2A and -2B

✓ Peer-reviewed alzhub usefulness score 45 out of 100. The Journal of biological chemistry 1995-03-01

Microtubule-associated protein tau is abnormally hyperphosphorylated in the brain of patients with Alzheimer disease and in this form is the major protein subunit of the paired helical filaments (PHF), the most prominent lesion of the disease. 4 key findings →

Evidence: low

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

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 27,780 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 →

Newest studies, as a dated timeline →    Atom feed