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Research

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

Find studies

Showing 1,251–1,275 of 1,346 studies (page 51 of 54) · 27,380 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; 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.

Evidence for physiological down-regulation of brain oxidative phosphorylation in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Experimental neurology 1996-11-01

In vivo imaging of patients with Alzheimer's disease using positron emission tomography (PET) demonstrates progressive reductions in brain glucose metabolism and blood flow in relation to dementia severity, more so in association than primary cortical regions. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Differential distribution of laminins in Alzheimer disease and normal human brain tissue

✓ Peer-reviewed alzhub usefulness score 35 out of 100. Journal of neuroscience research 2002-07-01

Immunocytochemistry, Western blotting, and RT-PCR were used to identify the isoforms of laminin expressed in the Alzheimer disease, but not in normal human brain tissue. 5 key findings →

Evidence: low

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

Cerebrovascular smooth muscle cells internalize Alzheimer amyloid beta protein via a lipoprotein pathway: implications for cerebral amyloid angiopathy

✓ Peer-reviewed alzhub usefulness score 35 out of 100. Laboratory investigation; a journal of technical methods and pathology 1997-08-01

Cerebral amyloid angiopathy (CAA) is caused by the cerebrovascular deposition of Alzheimer amyloid beta protein (Abeta) and shows an increased incidence in carriers of the apolipoprotein E (APOE) epsilon4 genotype. 1 key finding →

Evidence: low

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

Redox proteomics identification of specifically carbonylated proteins in the hippocampi of triple transgenic Alzheimer's disease mice at its earliest pathological stage

✓ Peer-reviewed alzhub usefulness score 35 out of 100. Journal of proteomics 2015-04-15

Alzheimer's disease (AD) is the most common cause of dementia in the elderly population. 5 key findings →

Evidence: low

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

Microglial activation induced by factor(s) contained in sera from Alzheimer-related ApoE genotypes

✓ Peer-reviewed alzhub usefulness score 35 out of 100. Journal of neuroscience research 1998-11-01

The risk of developing AD definitely increases with (a) age, (b) head injuries, (c) family history of AD or Down syndrome, (d) sex (higher prevalence of AD in women), (e) vascular disease, (f) exposure to environmental toxins, (g) infectious processes, or (h) changes in immune function, and recent advances in molecular genetics have suggested that genetic predisposition (i) can be considered one of the most important risk factors in the development of AD. 5 key findings →

Evidence: low

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

The Co-oligomers of Aβ42 and Human Islet Amyloid Polypeptide Exacerbate Neurotoxicity and Alzheimer-like Pathology at Cellular Level

✓ Peer-reviewed alzhub usefulness score 35 out of 100. Neuroscience 2024-04-09

The Aβ hypothesis has long been central to Alzheimer's disease (AD) theory, with a recent surge in attention following drug approvals targeting Aβ plaque clearance. 4 key findings →

Evidence: low

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

Aducanumab-Related Amyloid-Related Imaging Abnormalities: Paean or Lament?

✓ Peer-reviewed alzhub usefulness score 35 out of 100. Clinical nuclear medicine 2022-04-22

We believe that the amyloid-PET scans, perceived as showing decreasing amyloid deposits, are an expression of increased cerebral cell death due to aducanumab treatment, so that with time one should instead expect a worsening and not an improvement in the treated patients' condition. 1 key finding →

Evidence: low

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

Unraveling the conformational landscape of amyloid precursor protein intracellular domain

✓ Peer-reviewed alzhub usefulness score 35 out of 100. Biophysical Journal 2025-08-15

The amyloid precursor protein intracellular domain (AICD), a cleavage product of amyloid precursor protein implicated in Alzheimer disease and amyloid lateral sclerosis, is a functionally important but structurally elusive intrinsically disordered protein. 2 key findings →

Evidence: low

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

Influence of Ibuprofen on glycerophospholipids and sphingolipids in context of Alzheimer´s Disease

✓ Peer-reviewed alzhub usefulness score 35 out of 100. Biomedicine & Pharmacotherapy 2025-03-11

Alzheimer's disease (AD) is a multifactorial disorder associated with neuroinflammation, elevated oxidative stress, lipid alterations as well as amyloid-deposits and the formation of neurofibrillary tangles. 5 key findings →

Evidence: low

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

Layer-Specific Colocalization of Microglia with Amyloid Plaques in the Middle Temporal Gyrus Predicts Cognitive Decline in Alzheimer's Disease

✓ Peer-reviewed alzhub usefulness score 35 out of 100. Aging and Disease 2025-01-01

Alzheimer's disease (AD), the most common form of dementia, is marked by cognitive decline and amyloid-beta (Aβ) plaque deposition in the brain. 2 key findings →

Evidence: low

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

The spleen–brain axis in Alzheimer's disease and related dementias: Integrating immune and metabolic regulation

✓ Peer-reviewed alzhub usefulness score 35 out of 100. Alzheimer s & Dementia 2026-03-01

Emerging evidence highlights the central role of peripheral immune-metabolic regulation in the pathogenesis of Alzheimer's disease and related dementias (ADRD). 5 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 27,380 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