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Research

31,380 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 26–50 of 64 studies with an author at University of California, San Francisco (US) (page 2 of 3) · 31,380 in the whole library · How the 0–100 score works

Download bibliography of these 64 studies, in this order: BibTeX (.bib) · RIS (.ris)

Showing 64 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.

Other institutions

From OpenAlex; 16,851 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.

Posterior cingulate glucose metabolism, hippocampal glucose metabolism, and hippocampal volume in cognitively normal, late-middle-aged persons at 3 levels of genetic risk for Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 58 out of 100. JAMA neurology 2013-03-01

Although there were no significant differences among the 3 groups of participants in their clinical ratings, neuropsychological test scores, hippocampal volumes (P = .60), or hippocampal glucose metabolism measurements (P = .12), there were significant group differences in their posterior cingulate glucose metabolism measurements (P = .001). 2 key findings →

Design: cross-sectional Participants: 31 Evidence: low

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

High complement levels in astrocyte-derived exosomes of Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 58 out of 100. Annals of neurology 2018-03-10

Astrocytes fulfill neuronal trophic roles normally, but are transformed in Alzheimer disease (AD) into A1-type reactive astrocytes that may destroy neurons through unknown mechanisms. 2 key findings →

Participants: 28 Evidence: low

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

Association of brain amyloid-β with cerebral perfusion and structure in Alzheimer's disease and mild cognitive impairment

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Brain : a journal of neurology 2014-03-12

Patients with Alzheimer's disease have reduced cerebral blood flow measured by arterial spin labelling magnetic resonance imaging, but it is unclear how this is related to amyloid-β pathology. 4 key findings →

Participants: 51 Evidence: low

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

Apolipoprotein E: Cholesterol Transport Protein with Expanding Role in Cell Biology

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Science 1988-04-29

Apolipoprotein E is a plasma protein that serves as a ligand for low density lipoprotein receptors and, through its interaction with these receptors, participates in the transport of cholesterol and other lipids among various cells of the body.

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

Autosomal dominant and sporadic late onset Alzheimer's disease share a common in vivo pathophysiology

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Brain : a journal of neurology 2022-10-01

The extent to which the pathophysiology of autosomal dominant Alzheimer's disease corresponds to the pathophysiology of 'sporadic' late onset Alzheimer's disease is unknown, thus limiting the extrapolation of study findings and clinical trial results in autosomal dominant Alzheimer's disease to late onset Alzheimer's disease. 3 key findings →

Participants: 559 Evidence: low

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

A cross-sectional study of α-synuclein seed amplification assay in Alzheimer's disease neuroimaging initiative: Prevalence and associations with Alzheimer's disease biomarkers and cognitive function

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Alzheimer's & dementia : the journal of the Alzheimer's Association 2024-05-21

Alzheimer's disease (AD) pathology is defined by β-amyloid (Aβ) plaques and neurofibrillary tau, but Lewy bodies (LBs; 𝛼-synuclein aggregates) are a common co-pathology for which effective biomarkers are needed. 4 key findings →

Evidence: low

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

Association of Sleep and β-Amyloid Pathology Among Older Cognitively Unimpaired Adults

✓ Peer-reviewed alzhub usefulness score 55 out of 100. JAMA network open 2021-07-01

Amyloid PET and sleep duration information was acquired on 4425 cognitively unimpaired participants (mean [SD] age, 71.3 [4.7] years; 2628 [59.4%] female; 1509 [34.1%] tested Aβ positive). 4 key findings →

Design: cross-sectional Evidence: low

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

Effect of apolipoprotein E on biomarkers of amyloid load and neuronal pathology in Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Annals of neurology 2010-03-01

Low CSF Abeta(1-42) (surrogate for Abeta amyloid load) is more closely linked to the presence of APOE epsilon4 than to clinical status. 3 key findings →

Participants: 399 Evidence: low

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

Binding of human apolipoprotein E to synthetic amyloid beta peptide: isoform-specific effects and implications for late-onset Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 54 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1993-09-01

Apolipoprotein E (apoE), a plasma apolipoprotein that plays a central role in lipoprotein metabolism, is localized in the senile plaques, congophilic angiopathy, and neurofibrillary tangles of Alzheimer disease. 3 key findings →

Evidence: low

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

Cargo proteins of plasma astrocyte-derived exosomes in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 52 out of 100. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 2016-08-10

Efficient intercellular transfer of RNAs, proteins, and lipids as protected exosomal cargo has been demonstrated in the CNS, but distinct physiologic and pathologic roles have not been well defined for this pathway. 3 key findings →

Evidence: low

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

Association of Early-Onset Alzheimer Disease With Elevated Low-Density Lipoprotein Cholesterol Levels and Rare Genetic Coding Variants of APOB

✓ Peer-reviewed alzhub usefulness score 51 out of 100. JAMA neurology 2019-07-01

Elevated LDL-C levels were associated with higher probability of having EOAD, and EOAD cases were enriched for rare coding variants in APOB, which codes for the major protein of LDL-C. 3 key findings →

Evidence: low

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

Central Nervous System Lipoproteins: ApoE and Regulation of Cholesterol Metabolism

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Arteriosclerosis, thrombosis, and vascular biology 2016-05-12

ApoE on high-density lipoproteins is primarily responsible for lipid transport and cholesterol homeostasis in the central nervous system (CNS). 1 key finding →

Evidence: low

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

Comparative profiling of cortical gene expression in Alzheimer's disease patients and mouse models demonstrates a link between amyloidosis and neuroinflammation

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Scientific reports 2017-12-19

Alzheimer's disease (AD) is the most common form of dementia, characterized by accumulation of amyloid β (Aβ) and neurofibrillary tangles. 4 key findings →

Evidence: low

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

DNA methylation age from peripheral blood predicts progression to Alzheimer’s disease, white matter disease burden, and cortical atrophy

✓ Peer-reviewed alzhub usefulness score 50 out of 100. npj Dementia 2025-05-27

Cross-sectional studies suggest a limited relationship between accelerated epigenetic aging derived from epigenetic clocks, and Alzheimer's disease (AD) pathophysiology or risk. 3 key findings →

Design: cross-sectional Evidence: moderate

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

Apolipoprotein E is a kinetic but not a thermodynamic inhibitor of amyloid formation: implications for the pathogenesis and treatment of Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1995-01-01

The apolipoprotein E4 (APOE4) allele is associated with an early age of onset of the nonfamilial form of Alzheimer disease (AD) and with increased beta protein amyloid deposition in the brain. 3 key findings →

Evidence: low

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

Reversal of Alzheimer's-like pathology and behavior in human APP transgenic mice by mutation of Asp664

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2006-04-25

The deficits characteristic of Alzheimer's disease (AD) are believed to result, at least in part, from the neurotoxic effects of beta-amyloid peptides, a set of 39-43 amino acid fragments derived proteolytically from beta-amyloid precursor protein (APP). 4 key findings →

Evidence: low

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

Apolipoprotein E4 domain interaction mediates detrimental effects on mitochondria and is a potential therapeutic target for Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 48 out of 100. The Journal of biological chemistry 2010-11-30

Apolipoprotein (apo) E4 is the major genetic risk factor for late-onset Alzheimer disease (AD). 4 key findings →

Evidence: low

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

Modulation of Alzheimer-like synaptic and cholinergic deficits in transgenic mice by human apolipoprotein E depends on isoform, aging, and overexpression of amyloid beta peptides but not on plaque formation

✓ Peer-reviewed alzhub usefulness score 48 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2002-12-01

The most frequent human apolipoprotein (apo) E isoforms, E3 and E4, differentially affect Alzheimer's disease (AD) risk (E4 > E3) and age of onset (E4 < E3). 1 key finding →

Evidence: low

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

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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
  • Randomized / 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
  • Multicenter 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 31,380 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 31,380 records, built mostly from automated pulls of Europe PMC (65.6% of the library) and OpenAlex (16.2%), 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.

1,048 records (3.3% of the library) are not peer-reviewed — 973 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    Where this research is being discussed: events