alzhub.org
Get help now — free helplines

You can call any of these for free. You do not need a diagnosis, an appointment, or a crisis to call — questions and plain exhaustion are reasons enough.

  • Alzheimer's Association 24/7 Helpline 800-272-3900 24 hours a day, 365 days a year Free, confidential support and information for people with dementia, caregivers, families and the public. Master's-level clinicians. Also Spanish.
  • 988 Suicide & Crisis Lifeline 988 24/7 Call or text 988, or chat at 988lifeline.org. For anyone in emotional distress or a mental-health crisis, including caregivers.
  • Alzheimer's Foundation of America (AFA) Helpline 866-232-8484 9:00 am - 9:00 pm ET, seven days a week Licensed social workers providing support, info and referrals. Also text message and web chat. Text: 646-586-5283

In a medical emergency, call 911. More numbers, and what each line does, on the help page.

Research

28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 576–600 of 900 studies · free to read (page 24 of 36) · 28,180 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 900 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; 13,658 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.

Differences in amyloid PET positivity based on ethnoracial group and social determinants of health: The new IDEAS study

✓ Peer-reviewed alzhub usefulness score 46 out of 100. Alzheimer s & Dementia 2026-05-01

Among 5757 participants (21.7% Black, 20.3% Latinx, 58.1% AORE), we found lower odds of amyloid positivity in Black (odds ratio [OR]: 0.72, 95% confidence interval [CI]: 0.62-0.83) and Latinx (OR: 0.78, 95% CI: 0.67-0.91) compared to AORE. 4 key findings →

Participants: 5,757 Evidence: moderate

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

Time Course and Severity of Cognitive Changes as a Function of Aβ Positivity and APOE Genotype in Alzheimer Disease

✓ Peer-reviewed alzhub usefulness score 46 out of 100. Neurology 2025-06-27

We analyzed data from 1,542 participants (mean age = 72.2 years, SD = 7.2; 50.8% female; mean education = 16.3 years, SD = 2.6) and found that APOE4 was associated with steeper declines in episodic memory as a function of Aβ duration. 5 key findings →

Participants: 1,542 Evidence: low

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

Multi-functional role of apolipoprotein E in neurodegenerative diseases

✓ Peer-reviewed alzhub usefulness score 46 out of 100. Frontiers in Aging Neuroscience 2025-01-29

Genetic diversity in the apolipoprotein E (ApoE) gene has been identified as the major susceptibility genetic risk factor for sporadic Alzheimer’s disease (SAD). 1 key finding →

Evidence: low

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

Retinal Imaging Findings in Carriers With PSEN1-Associated Early-Onset Familial Alzheimer Disease Before Onset of Cognitive Symptoms

✓ Peer-reviewed alzhub usefulness score 46 out of 100. JAMA ophthalmology 2021-01-01

These findings suggest that OCT can detect functional and morphologic changes in the retina of carriers of familial Alzheimer disease who are cognitively unimpaired several years before clinical onset, suggesting that OCT findings and retinal vascular parameters may be biomarkers prior to the onset of cognitive decline. 4 key findings →

Design: cross-sectional Evidence: low

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

The influence of Alzheimer disease family history and apolipoprotein E epsilon4 on mesial temporal lobe activation

✓ Peer-reviewed alzhub usefulness score 45 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2006-05-01

First-degree family history of sporadic Alzheimer disease (AD) and the apolipoprotein E epsilon4 (APOE4) are risk factors for developing AD. 1 key finding →

Evidence: low

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

Neuropathology and apolipoprotein E profile of aged chimpanzees: implications for Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1994-09-01

Neuropathological findings in three aged chimpanzees were compared with those in rhesus monkeys and individuals with Alzheimer disease. 3 key findings →

Evidence: low

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

High-fat diet-induced deregulation of hippocampal insulin signaling and mitochondrial homeostasis deficiences contribute to Alzheimer disease pathology in rodents

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Biochimica et biophysica acta 2015-05-21

Global obesity is a pandemic status, estimated to affect over 2 billion people, that has resulted in an enormous strain on healthcare systems worldwide. 3 key findings →

Evidence: low

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

Metabolic networks underlying cognitive reserve in prodromal Alzheimer disease: a European Alzheimer disease consortium project

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Journal of nuclear medicine : official publication, Society of Nuclear Medicine 2013-04-16

The clusters of significant depression and compensation were further used as volumetric regions of interest (ROIs) in a brain interregional correlation analysis in each prodromal AD subgroup to explore metabolic connectivity. 3 key findings →

Evidence: low

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

The Link between Oxidative Stress, Mitochondrial Dysfunction and Neuroinflammation in the Pathophysiology of Alzheimer's Disease: Therapeutic Implications and Future Perspectives

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Antioxidants (Basel, Switzerland) 2022-10-31

Alzheimer's disease (AD), the most common form of dementia, has increasing incidence, increasing mortality rates, and poses a huge burden on healthcare. 1 key finding →

Evidence: low

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

Aβ mediates F-actin disassembly in dendritic spines leading to cognitive deficits in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 45 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2017-12-15

Dendritic spine structure is defined by filamentous actin (F-actin) and we observed depolymerization of synaptosomal F-actin accompanied by increased globular-actin (G-actin) at as early as 1 month of age in a mouse model of AD (APPswe/PS1ΔE9, male mice). 3 key findings →

Evidence: low

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

Amyloid-beta deposits lead to retinal degeneration in a mouse model of Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Investigative ophthalmology & visual science 2008-06-19

Retinas of transgenic mice harboring a mutant presenilin (PS1) and a mutant APP gene were processed for TUNEL and immunohistochemistry with antibodies against APP, amyloid-beta, monocyte chemotactic protein (MCP)-1, and F4/80. 4 key findings →

Evidence: low

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

MicroRNA-298 and microRNA-328 regulate expression of mouse beta-amyloid precursor protein-converting enzyme 1

✓ Peer-reviewed alzhub usefulness score 45 out of 100. The Journal of biological chemistry 2008-11-05

MicroRNAs (miRNAs) are key regulatory RNAs known to repress mRNA translation through recognition of specific binding sites located mainly in their 3'-untranslated region (UTR). 4 key findings →

Evidence: low

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

Familial Alzheimer disease-linked mutations specifically disrupt Ca2+ leak function of presenilin 1

✓ Peer-reviewed alzhub usefulness score 45 out of 100. The Journal of clinical investigation 2007-04-12

Mutations in presenilins are responsible for approximately 40% of all early-onset familial Alzheimer disease (FAD) cases in which a genetic cause has been identified. 4 key findings →

Evidence: low

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

The amyloid precursor protein: a biochemical enigma in brain development, function and disease

✓ Peer-reviewed alzhub usefulness score 45 out of 100. FEBS letters 2013-05-16

For 20 years the amyloid cascade hypothesis of Alzheimer disease (AD) has placed the amyloid-β peptide (Aβ), formed from the amyloid precursor protein (APP), centre stage in the process of neurodegeneration. 4 key findings →

Evidence: low

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

↑ 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.

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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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