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Research

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

Find studies

Showing 1,576–1,600 of 1,615 studies in Genetics (page 64 of 65) · 27,380 in the whole library · How the 0–100 score works

Browse by subject, author or institution

Each number is how many studies that link shows, with your other filters kept.

Other 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.

What “Genetics” covers

Genetics — Inherited risk: APOE and the other risk genes, and what they do and don't tell you.

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.

Feature harmonization reveals that apparent cross-cohort differences in tau-positivity prediction reflect variable availability and cohort stage structure

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-10-21

In the primary matched-feature comparison, reference areas under the receiver operating characteristic curve (AUCs) were 0.851 for ADNI tau90, 0.860 for ADNI tau180, and 0.933 for OASIS3 tau180. 3 key findings →

Evidence: moderate

Full summary, score breakdown and related studies → Original source

A rapid, genetically-tractable human iPSC-derived model for studying tissue-resident macrophage biology in Alzheimer’s and other diseases

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-12

Large-scale genetic and preclinical studies strongly implicate myeloid cells, particularly brain-resident macrophages, in the pathogenesis of Alzheimer’s disease (AD). 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source

Turbulent dynamics and in silico perturbation-based measures are disrupted across biological stages of Alzheimers disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-10-13

According to the AT(N) framework, Alzheimers disease (AD) can be biologically characterised by amyloid deposition, tau pathology, and neurodegeneration, yet how these processes relate to whole-brain dynamics remains unclear. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Location-specific Longitudinal Patterns of Subcortical and Lobar Cerebral Microhemorrhages in Preclinical Alzheimer Disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-10-13

Emerging evidence and expert opinion suggest that subcortical microhaemorrhages may be less closely related to cerebral amyloidosis than lobar lesions and may therefore warrant separate consideration in anti-amyloid treatment eligibility criteria. 5 key findings →

Design: longitudinal study Participants: 1,146 Evidence: moderate

Full summary, score breakdown and related studies → Original source

Clinical utility of plasma APOE proteotyping for Alzheimer’s disease risk and prognosis

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-10-11

Plasma APOE4 proteotyping accurately distinguished genotype-defined APOE ε4 carrier status and copy number while demonstrating AD-related associations comparable to DNA genotyping. 1 key finding →

Design: cross-sectional Evidence: low

Full summary, score breakdown and related studies → Original source

Mapping polygenic risk scores to brain cells: insights for neurodegenerative diseases

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-10-11

Neurodegenerative diseases (NDDs) are driven by multiple related yet distinct pathological processes that evolve over decades, resulting in substantial clinical and neuropathological heterogeneity. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Locus coeruleus intensity as a marker of early-stage Alzheimer’s disease: associations with plasma pTau 217 and memory

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-10-09

These findings support MRI-derived LC intensity as a marker of early AD-related processes and suggest that LC intensity may provide complementary information not captured by plasma pTau 217 alone. 4 key findings →

Design: longitudinal study Participants: 163 Evidence: moderate

Full summary, score breakdown and related studies → Original source

The Alzheimer's disease-associated rs28834970 variant in PTK2B impairs electrical activity and regulates Tau phosphorylation and APP processing in human neuronal cultures

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-30

The rs28834970 regulatory variant was identified as the most functionally relevant in our model, with the C risk allele promoting transcription factor C/EBPβ binding within a cis-regulatory element. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Single-Nucleus Profiling Reveals Neuronal Metabolic Collapse During the Transition to Alzheimer’s Disease Dementia

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-28

Current Alzheimer’s disease (AD) neuropathological metrics, including Thal phasing, and Braak staging, often do not accurately predict cognitive status: many cognitively resilient individuals have substantial pathological burdens, whereas some patients with dementia show minimal classical AD pathology. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Ms4a4a loss preferentially remodels microglia with limited, compartment-specific effects across central and peripheral immune compartments in 5xFAD mice

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-27

These findings identify microglia as the immune population most strongly remodeled by Ms4a4a loss in the setting of amyloid pathology. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

A family-aware All of Us benchmark for polygenic prediction and genomic machine learning

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-10-26

Polygenic risk scores (PRSs) have improved substantially in predictive performance, yet results remain difficult to compare across studies that differ in cohorts, phenotype definitions, and evaluation procedures. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Structured Metabolic Genetic Axes Reveal Distinct Lipid and Ketone-Body Programs in Alzheimer’s and Parkinson’s Disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-10-19

Structured metabolic genetic axes reveal selective and biologically distinct links between circulating metabolism and neurodegenerative disease, providing a framework for mechanism-focused follow-up beyond single-metabolite association. 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source

Transcriptomic and phenotypic characterization of Alzheimer’s disease risk genes in neurons and astrocytes highlights shared and cell type specific cellular mechanisms

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-14

Genome-wide association studies have identified nearly 100 genetic loci that affect Alzheimer’s disease risk. 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Disease-Specific Perturbational Convergence Between Genetic-Risk and Disease-State Transcriptomic Signatures in Alzheimer's Disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-10-12

In the present analysis, genetic risk and end-stage AD pathology are largely decoupled at the level of individual genes and pathways but converge on a shared, pharmacologically modifiable response landscape. 1 key finding →

Participants: 3,202 Evidence: low

Full summary, score breakdown and related studies → Original source

Regional similarity to male-typical brain architecture links childhood ADHD to neurophysiological aging in later adulthood

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-09-29

Identifying early life biomarkers of suboptimal aging trajectories could help design interventions to delay or even prevent the onset of pathological conditions in older adulthood. 1 key finding →

Participants: 522 Evidence: low

Full summary, score breakdown and related studies → Original source

Large-Scale Genome-wide association study identified Shared Genetic Risk SNPs Correlates in Epilepsy and Alzheimer's Disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-09-23

Inverse-variance weighted MR indicated that genetically predicted focal epilepsy with hippocampal sclerosis was associated with increased odds of AD (OR=3.99, 95% CI 1.17–13.61; P=0.027). 5 key findings →

Participants: 803 Evidence: low

Full summary, score breakdown and related studies → Original source

Genetically predicted multisite chronic pain is associated with lower cognitive performance: a bidirectional Mendelian randomization study with NHANES contextual evidence

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-09-22

Chronic pain and cognitive impairment are rising ageing-related burdens. 4 key findings →

Design: longitudinal study Participants: 387,649 Evidence: moderate

Full summary, score breakdown and related studies → Original source

TDP-43 dysfunction induces cryptic circular RNAs in ALS/FTD

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-09-20

Nuclear depletion of TDP-43 is a defining pathological feature of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), leading to widespread RNA misprocessing, including the formation of cryptic exons. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Integration of cell-specific gene expression and chromatin accessibility facilitates localization of neurodegenerative risk in microglia

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-09-17

Genome-wide association studies (GWAS) have identified many loci that contribute to the risk of neurodegenerative diseases. 3 key findings →

Design: meta-analysis Evidence: high

Full summary, score breakdown and related studies → Original source

Disrupting SORL1-retromer endosomal recycling in mice drives the age-dependent neurodegenerative signature of Alzheimer's disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-30

MRI studies have mapped the atrophic signature that distinguishes Alzheimer's disease (AD), isolating regions differentially vulnerable to its age-dependent neurodegenerative process. 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

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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
  • 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