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Research

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

Find studies

Showing 576–600 of 1,593 studies · free to read · tagged Genetics (page 24 of 64) · 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)

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.

Lipid-associated macrophages' promotion of fibrosis resolution during MASH regression requires TREM2

✓ Peer-reviewed alzhub usefulness score 54 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2024-08-22

While macrophage heterogeneity during metabolic dysfunction-associated steatohepatitis (MASH) has been described, the fate of these macrophages during MASH regression is poorly understood. 4 key findings →

Evidence: low

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

Trem2 expression in microglia is required to maintain normal neuronal bioenergetics during development

✓ Peer-reviewed alzhub usefulness score 54 out of 100. Immunity 2023-12-29

Triggering receptor expressed on myeloid cells 2 (Trem2) is a myeloid cell-specific gene expressed in brain microglia, with variants that are associated with neurodegenerative diseases, including Alzheimer's disease. 4 key findings →

Evidence: low

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

Genome-wide RNAseq study of the molecular mechanisms underlying microglia activation in response to pathological tau perturbation in the rTg4510 tau transgenic animal model

✓ Peer-reviewed alzhub usefulness score 54 out of 100. Molecular neurodegeneration 2018-12-17

Activation of microglia, the resident immune cells of the central nervous system, is a prominent pathological hallmark of Alzheimer's disease (AD). 4 key findings →

Design: longitudinal study Evidence: moderate

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

Assessment of the Genetic Architecture of Alzheimer's Disease Risk in Rate of Memory Decline

✓ Peer-reviewed alzhub usefulness score 54 out of 100. Journal of Alzheimer's disease : JAD 2018-01-01

Many genetic studies for Alzheimer's disease (AD) have been focused on the identification of common genetic variants associated with AD risk and not on other aspects of the disease, such as age at onset or rate of dementia progression. 4 key findings →

Design: longitudinal study Evidence: moderate

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

Association between polygenic risk score of Alzheimer's disease and plasma phosphorylated tau in individuals from the Alzheimer's Disease Neuroimaging Initiative

✓ Peer-reviewed alzhub usefulness score 54 out of 100. Alzheimer's research & therapy 2021-01-08

Recent studies suggest that plasma phosphorylated tau181 (p-tau181) is a highly specific biomarker for Alzheimer's disease (AD)-related tau pathology. 4 key findings →

Participants: 818 Evidence: low

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

Assessment of executive function declines in presymptomatic and mildly symptomatic familial frontotemporal dementia: NIH-EXAMINER as a potential clinical trial endpoint

✓ Peer-reviewed alzhub usefulness score 54 out of 100. Alzheimer's & dementia : the journal of the Alzheimer's Association 2020-01-01

Identifying clinical measures that track disease in the earliest stages of frontotemporal lobar degeneration (FTLD) is important for clinical trials. 4 key findings →

Participants: 31 Evidence: low

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

Significant association between SCN8A and Alzheimer disease in Puerto Ricans

✓ Peer-reviewed alzhub usefulness score 54 out of 100. Alzheimer s & Dementia 2025-12-01

) within the first intron of SCN8A on chromosome 12 (Figure 1), overlapping a significant region in the previous admixture mapping analysis. eHiCA revealed more and stronger interactions between rs4761988 and SLC4A8, SCN8A and FIGNL2 in EU compared to AF genome (Figure 2), consistent with the admixture mapping result. 4 key findings →

Design: meta-analysis Participants: 867 Evidence: high

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

Liver Diseases and Brain Disorders: Genetic Mechanisms and Biomarker Pathways in a Prospective Cohort Study From the UK Biobank

✓ Peer-reviewed alzhub usefulness score 54 out of 100. Journal of Neurochemistry 2025-04-01

Population-based evidence directly linking liver diseases to brain disorders is limited, and its genetic and biochemical associations remain unclear. 2 key findings →

Design: cohort study Participants: 59 Evidence: moderate

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

Systematic review of genetic association studies in people with Lewy body dementia

✓ Peer-reviewed alzhub usefulness score 54 out of 100. International journal of geriatric psychiatry 2020-01-16

Eight thousand five hundred twenty-one articles were screened, and 75 articles were eligible to be included. 2 key findings →

Design: systematic review Evidence: high

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

Interaction between variants in CLU and MS4A4E modulates Alzheimer's disease risk

✓ Peer-reviewed alzhub usefulness score 54 out of 100. Alzheimer's & dementia : the journal of the Alzheimer's Association 2015-10-09

We replicated the CLU-MS4A4E interaction in a large case-control series and observed APOE ε4 and possible dominant effect. 1 key finding →

Design: meta-analysis Evidence: high

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

Plasma tau correlates with basal forebrain atrophy rates in people at risk for Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Neurology 2019-12-04

Increased concentrations of baseline plasma t-tau may predict in vivo structural BFCS atrophy progression in older adults at risk for AD, independently of β-amyloid status and APOE genotype. 3 key findings →

Participants: 251 Evidence: moderate

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

Apolipoprotein E and Alzheimer disease: pathobiology and targeting strategies

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Nature reviews. Neurology 2019-07-31

Polymorphism in the apolipoprotein E (APOE) gene is a major genetic risk determinant of late-onset Alzheimer disease (AD), with the APOE*ε4 allele conferring an increased risk and the APOE*ε2 allele conferring a decreased risk relative to the common APOE*ε3 allele. 2 key findings →

Evidence: low

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

Increased amyloid beta-peptide deposition in cerebral cortex as a consequence of apolipoprotein E genotype in late-onset Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1993-10-01

Amyloid beta-peptide (A beta) deposition in senile plaques and cerebral vessels is a neuropathological feature of Alzheimer disease (AD). 2 key findings →

Evidence: low

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

PGC-1alpha expression decreases in the Alzheimer disease brain as a function of dementia

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Archives of neurology 2009-03-01

Therapeutic preservation of neuronal PGC-1alpha expression promotes the nonamyloidogenic processing of amyloid precursor protein precluding the generation of amyloidogenic Abeta peptides. 4 key findings →

Design: case-control study Evidence: moderate

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

Prevalence of vitamin d insufficiency in patients with Parkinson disease and Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Archives of neurology 2008-10-01

This report of 25(OH)D concentrations in a predominantly white PD cohort demonstrates a significantly higher prevalence of hypovitaminosis in PD vs both healthy controls and patients with AD. 3 key findings →

Participants: 97 Evidence: moderate

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

Apolipoprotein E: Structural Insights and Links to Alzheimer Disease Pathogenesis

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Neuron 2020-11-10

Apolipoprotein E (ApoE) is of great interest due to its role as a cholesterol/lipid transporter in the central nervous system (CNS) and as the most influential genetic risk factor for Alzheimer disease (AD). 4 key findings →

Evidence: low

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

Enhanced risk for Alzheimer disease in persons with type 2 diabetes and APOE epsilon4: the Cardiovascular Health Study Cognition Study

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Archives of neurology 2008-01-01

These data suggest that having both diabetes and APOE epsilon4 increases the risk of dementia, especially for AD and mixed AD. 2 key findings →

Evidence: moderate

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.

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