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Research

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

Find studies

Showing 176–200 of 205 studies with an author at Harvard University (US) · tagged Genetics (page 8 of 9) · 31,380 in the whole library · How the 0–100 score works

Download bibliography of these 205 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.

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.

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

Insomnia symptom severity and cognitive performance: Moderating role of APOE genotype

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Alzheimer's & dementia : the journal of the Alzheimer's Association 2021-07-26

We evaluated whether insomnia symptom severity was associated with cognitive function, and whether this relationship was modified by biomarkers associated with Alzheimer's disease risk. 4 key findings →

Evidence: low

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

Systematic analysis of cellular cross-talk reveals a role for SEMA6D-TREM2 regulating microglial function in Alzheimer’s disease

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Science Translational Medicine 2025-07-30

Cellular cross-talk, mediated by membrane receptors and their ligands, is crucial for brain homeostasis and can contribute to neurodegenerative diseases such as Alzheimer’s disease (AD). 4 key findings →

Evidence: low

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

Mapping of the gene encoding the beta-amyloid precursor protein and its relationship to the Down syndrome region of chromosome 21

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1988-11-01

The gene encoding the beta-amyloid precursor protein has been assigned to human chromosome 21, as has a gene responsible for at least some cases of familial Alzheimer disease. 2 key findings →

Evidence: low

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

Presenilin mutations in familial Alzheimer disease and transgenic mouse models accelerate neuronal lysosomal pathology

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Journal of neuropathology and experimental neurology 2004-08-01

The neuronal lysosomal system is a major degradative pathway, induced by cell stress and closely linked to Alzheimer disease (AD) and other neurodegenerative diseases. 4 key findings →

Evidence: low

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

Exploring immediate responses to APOE ε 4/ε4 genotype and Alzheimer's disease risk disclosure in Latinos

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Journal of Alzheimer s Disease 2026-03-30

Among most Latinos in northern Manhattan who learned they had an APOE ε4/ε4 genotype, disclosure did not provoke elevated levels of distress. 3 key findings →

Participants: 61 Evidence: low

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

Polygenic Risk Scores for Incident Dementia in the Multi‐Ethnic Study of Atherosclerosis

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Genetic Epidemiology 2026-06-23

We found comparable associations between dementia and PRS when comparing a C+T method with only 15 SNPs and PRS derived from Bayesian models that include > 800,000 SNPs (HR 5e‐08 = 1.18, 95% CI: 1.08–1.28; HR CSx = 1.17, 95% CI: 1.07−1.27). 3 key findings →

Evidence: low

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

Role of the low-density lipoprotein receptor-related protein in beta-amyloid metabolism and Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Archives of neurology 2000-05-01

Deposition of beta-amyloid (A beta), a metabolite of approximately 4 kd of the amyloid precursor protein, is a critical pathological feature in Alzheimer disease. 5 key findings →

Evidence: low

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

APP mutations in the Aβ coding region are associated with abundant cerebral deposition of Aβ38

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Acta neuropathologica 2012-11-13

Aβ is the main component of amyloid deposits in Alzheimer disease (AD) and its aggregation into oligomers, protofibrils and fibrils is considered a seminal event in the pathogenesis of AD. 2 key findings →

Evidence: low

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

VCP disease associated with myopathy, Paget disease of bone and frontotemporal dementia: review of a unique disorder

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Biochimica et biophysica acta 2008-09-18

Inclusion body myopathy (IBM) associated with Paget disease of the bone (PDB) and frontotemporal dementia (FTD) (now called IBMPFD), is a progressive autosomal dominant disorder that was recently identified as being caused by mutations in the VCP (p97 or CDC48) gene which plays a key role in the ubiquitin-proteasome dependent degradation of cytosolic proteins and in the retro translocation of misfolded proteins from the endoplasmic reticulum into the cytoplasm. 4 key findings →

Evidence: low

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

Plasma lipidome dysregulation in frontotemporal dementia reveals shared, genotype‐specific, and severity‐linked alterations

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Alzheimer s & Dementia 2025-09-01

FTD subjects exhibited increased plasma levels of gangliosides (GM3(d18:1_16:0), GM3(d18:1_24:1)), ceramide Cer(d18:1_23:0), and select polyunsaturated triacylglycerols. 5 key findings →

Evidence: low

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

Association of a haplotype for tumor necrosis factor in siblings with late-onset Alzheimer disease: the NIMH Alzheimer Disease Genetics Initiative

✓ Peer-reviewed alzhub usefulness score 42 out of 100. American journal of medical genetics 2000-12-01

Tumor necrosis factor (TNF), a proinflammatory cytokine, may be involved in the pathogenesis of Alzheimer disease (AD) based on observations that senile plaques have been found to upregulate proinflammatory cytokines. 3 key findings →

Evidence: low

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

A novel C. elegans model for MAPT/Tau spreading reveals genes critical for endolysosomal integrity and seeded MAPT/Tau aggregation

✓ Peer-reviewed alzhub usefulness score 42 out of 100. Autophagy 2025-08-25

The spreading of MAPT/Tau pathology is closely associated with the progression of neurodegeneration and cognitive decline in Alzheimer disease and other tauopathies. 5 key findings →

Evidence: low

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

Presenilin-1 Familial Alzheimer Mutations Impair γ-Secretase Cleavage of APP Through Stabilized Enzyme–Substrate Complex Formation

✓ Peer-reviewed alzhub usefulness score 42 out of 100. Biomolecules 2025-07-01

Familial Alzheimer's disease (FAD) is caused by dominant missense mutations in amyloid precursor protein (APP) and presenilin-1 (PSEN1), the catalytic component of γ-secretase that generates amyloid β-peptides (Aβ) from the APP C-terminal fragment C99. 3 key findings →

Evidence: low

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

Relationship between APOE Genotype Status and Imaging Features in Patients with Alzheimer Disease Being Considered for Antiamyloid β Therapy

✓ Peer-reviewed alzhub usefulness score 41 out of 100. American Journal of Neuroradiology 2026-03-01

A total of 85 patients were included in the study with rare genotypes excluded from analysis (3 patients). 5 key findings →

Participants: 85 Evidence: moderate

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

APOE ε4 linked effects on clinical features and neuropathology in dementia with Lewy bodies

✓ Peer-reviewed alzhub usefulness score 39 out of 100. Alzheimer s & Dementia 2025-10-01

In analyses of APOE ε4 carriers, dosage, and genetic risk score, APOE ε4 was associated with lower odds of fluctuating cognition and parkinsonism and higher odds of visual hallucinations. 5 key findings →

Evidence: low

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

Alzheimer-mutant γ-secretase complexes stall amyloid β-peptide production

✓ Peer-reviewed alzhub usefulness score 39 out of 100. eLife 2025-02-11

Missense mutations in the amyloid precursor protein (APP) and presenilin-1 (PSEN1) cause early-onset familial Alzheimer’s disease (FAD) and alter proteolytic production of secreted 38-to-43-residue amyloid β-peptides (Aβ) by the PSEN1-containing γ-secretase complex, ostensibly supporting the amyloid hypothesis of pathogenesis. 3 key findings →

Evidence: low

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

Hormone replacement therapy in women and vascular risk factors modify the association of a multi‐ancestry polygenic risk score with Alzheimer disease and related traits

✓ Peer-reviewed alzhub usefulness score 38 out of 100. Alzheimer s & Dementia 2025-12-01

The AD PRS was associated with AD in the ADSP sample, with odds ratios per standard deviation ranging from 1.14 to 1.52 across ancestry groups and robust validation in independent cohorts (Figure 1). 5 key findings →

Evidence: low

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

On the association analysis of genome-sequencing data: A spatial clustering approach for partitioning the entire genome into nonoverlapping windows

✓ Peer-reviewed alzhub usefulness score 35 out of 100. Genetic epidemiology 2017-03-21

For the association analysis of whole-genome sequencing (WGS) studies, we propose an efficient and fast spatial-clustering algorithm. 2 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. 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