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Research

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

Find studies

Showing 776–800 of 1,593 studies · free to read · tagged Genetics (page 32 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.

Deficiency of TYROBP, an adapter protein for TREM2 and CR3 receptors, is neuroprotective in a mouse model of early Alzheimer's pathology

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Acta neuropathologica 2017-06-13

Conventional genetic approaches and computational strategies have converged on immune-inflammatory pathways as key events in the pathogenesis of late onset sporadic Alzheimer's disease (LOAD). 4 key findings →

Evidence: low

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

Loss of TREM2 rescues hyperactivation of microglia, but not lysosomal deficits and neurotoxicity in models of progranulin deficiency

✓ Peer-reviewed alzhub usefulness score 51 out of 100. The EMBO journal 2022-01-12

Haploinsufficiency of the progranulin (PGRN)-encoding gene (GRN) causes frontotemporal lobar degeneration (GRN-FTLD) and results in microglial hyperactivation, TREM2 activation, lysosomal dysfunction, and TDP-43 deposition. 4 key findings →

Evidence: low

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

Homozygous TREM2 mutation in a family with atypical frontotemporal dementia

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Neurobiology of aging 2014-04-18

TREM2 mutations were first identified in Nasu-Hakola disease, a rare autosomal recessive disease characterized by recurrent fractures because of bone cysts and presenile dementia. 4 key findings →

Evidence: low

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

Wild-type sTREM2 blocks Aβ aggregation and neurotoxicity, but the Alzheimer's R47H mutant increases Aβ aggregation

✓ Peer-reviewed alzhub usefulness score 51 out of 100. The Journal of biological chemistry 2021-01-01

TREM2 is a pattern recognition receptor, expressed on microglia and myeloid cells, detecting lipids and Aβ and inducing an innate immune response. 4 key findings →

Evidence: low

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

CSF concentrations of soluble TREM2 as a marker of microglial activation in HIV-1 infection

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Neurology(R) neuroimmunology & neuroinflammation 2018-11-07

CSF sTREM2 increased with systemic and CNS HIV-1 disease severity, with the highest levels found in patients with HIV-associated dementia (HAD). 4 key findings →

Design: cross-sectional Evidence: low

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

Alzheimer's disease-linked risk alleles elevate microglial cGAS-associated senescence and neurodegeneration in a tauopathy model

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Neuron 2024-09-30

The strongest risk factors for late-onset sporadic Alzheimer's disease (AD) include the ε4 allele of apolipoprotein E (APOE), the R47H variant of triggering receptor expressed on myeloid cells 2 (TREM2), and female sex. 4 key findings →

Evidence: low

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

Microglia at sites of atrophy restrict the progression of retinal degeneration via galectin-3 and Trem2

✓ Peer-reviewed alzhub usefulness score 51 out of 100. The Journal of experimental medicine 2024-01-30

Outer retinal degenerations, including age-related macular degeneration (AMD), are characterized by photoreceptor and retinal pigment epithelium (RPE) atrophy. 4 key findings →

Evidence: low

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

Interactions between apolipoprotein E, sex, and amyloid-beta on cerebrospinal fluid p-tau levels in the European prevention of Alzheimer's dementia longitudinal cohort study (EPAD LCS)

✓ Peer-reviewed alzhub usefulness score 51 out of 100. EBioMedicine 2022-08-27

The apolipoprotein E (APOE)ε4 allele is the strongest genetic risk factor for late-onset AD and is associated with aberrant cerebrospinal fluid levels (CSF) of total tau (t-tau), phosphorylated tau (p-tau), and amyloid-β (Aβ). 4 key findings →

Design: cohort study Evidence: moderate

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

TMEM106B, the risk gene for frontotemporal dementia, is regulated by the microRNA-132/212 cluster and affects progranulin pathways

✓ Peer-reviewed alzhub usefulness score 51 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2012-08-01

Frontotemporal lobar degeneration with TDP-43 inclusions (FTLD-TDP) is a fatal neurodegenerative disease with no available treatments. 4 key findings →

Evidence: low

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

Apolipoprotein E Mimetic Peptide CN-105 and Postoperative Delirium in Older Patients

✓ Peer-reviewed alzhub usefulness score 51 out of 100. JAMA Network Open 2026-04-03

Among 203 enrolled patients, 186 (mean [SD] age, 68.7 [5.2] years; 119 males [64.0%]) were randomized (137 to the CN-105 group, 49 to the placebo group) and underwent surgery. 5 key findings →

Design: clinical trial Evidence: high

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

Genetic drivers of hippocampal atrophy highlight the role of APOE functional variants and AD polygenicity in Mild Cognitive Impairment

✓ Peer-reviewed alzhub usefulness score 51 out of 100. NeuroImage Clinical 2025-01-01

• Longitudinal imaging-genetics study of hippocampal atrophy trajectories over 5 years in ADNI. • APOE -ε4 carriership and ApoE CSF proteomic quantitative trait loci are key genetic drivers of accelerated hippocampal atrophy in amyloid-positive MCI. • Genetic effects are stage-specific, with strongest associations during the prodromal phase of AD. • Sex differences in atrophy rates are observed, but do not significantly alter genetic influences. • Findings support the utility of APOE and functional genetic markers as stratification tools for early neurodegeneration in AD. 4 key findings →

Design: longitudinal study Participants: 1,051 Evidence: moderate

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

Elevated gonadotropins and risk of dementia in Chinese adults aged over 80: a cross-sectional study

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Frontiers in Aging Neuroscience 2025-10-17

Elevated FSH and reduced LH may be associated with poorer cognition and an increased risk of AD-D in very old Chinese adults, particularly in males. 5 key findings →

Design: cross-sectional Participants: 509 Evidence: moderate

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

Liver–metabolic stress, apolipoprotein E ε4, and cognition and amyloid burden: findings from the dementia platform Korea trial-ready registry

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Frontiers in Aging Neuroscience 2026-03-11

Routine liver–metabolic indices were associated with cognitive performance, while FIB-4 stage showed effect modification by APOE ε4 in relation to both cognition and amyloid PET SUVR. 4 key findings →

Design: longitudinal study Participants: 507 Evidence: moderate

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

Alzheimer’s disease polygenic risk’s association with all-cause dementia through the plasma metabolome in the UK Biobank study

✓ Peer-reviewed alzhub usefulness score 51 out of 100. GeroScience 2025-06-30

Higher AD PRS was associated with increased risks of all-cause dementia (HR: 1.75, 95% CI: 1.70-1.79, P < 0.001) and AD (HR: 2.02, 95% CI: 1.95-2.09, P < 0.001), with stronger effects in women for both outcomes when considering the main AD PRS which was related to APOE4 status. 4 key findings →

Participants: 249 Evidence: low

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

Cryptic splicing in synaptic and membrane excitability genes links TDP-43 loss to neuronal dysfunction

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Science Translational Medicine 2026-06-03

Using human stem cell-derived neurons, we show that TDP-43 reduction induces cryptic splicing and downregulation of these genes, resulting in impaired excitability and synaptic transmission. 1 key finding →

Evidence: low

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

Slowly progressive dementia caused by MAPT R406W mutations: longitudinal report on a new kindred and systematic review

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Alzheimer's research & therapy 2018-01-09

Dominance of 4R over three-repeat (exon 10-) tau isoforms contrasts with earlier reports of R406W patients and was not sufficiently explained by the presence of H1/H2 haplotypes in two of the autopsied patients. 3 key findings →

Design: systematic review Evidence: low

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

Multi-ancestry transcriptome-wide association study reveals shared and population-specific genetic effects in Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 50 out of 100. American Journal of Human Genetics 2026-04-30

Alzheimer disease (AD) risk differs across ancestral populations, yet most genetic studies have focused on non-Hispanic White (NHW) cohorts. 1 key finding →

Design: cross-sectional Participants: 751 Evidence: early

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

APOE-stratified genome-wide association analyses provide insights into the genetic etiology of Alzheimers's disease

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Nature genetics 2026-09-14

Among the more than 90 identified genetic risk loci for late-onset Alzheimer's disease (AD) and related dementias, the apolipoprotein E (APOE) gene ɛ2/ɛ3/ɛ4 polymorphisms remain the longstanding benchmark for genetic disease risk with a consistently large effect across studies 1-10 . 5 key findings →

Design: case-control Evidence: high

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

Reelin and ApoE receptors cooperate to enhance hippocampal synaptic plasticity and learning

✓ Peer-reviewed alzhub usefulness score 50 out of 100. The Journal of biological chemistry 2002-08-07

Two apolipoprotein E (apoE) receptors, the very low density lipoprotein (VLDL) receptor and apoE receptor 2 (apoER2), are also receptors for Reelin, a signaling protein that regulates neuronal migration during brain development. 3 key findings →

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.

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