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Research

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

Find studies

Showing 151–175 of 205 studies with an author at Harvard University (US) · tagged Genetics (page 7 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.

Multi-omic comparison of Alzheimer's variants in human ESC-derived microglia reveals convergence at APOE

✓ Peer-reviewed alzhub usefulness score 50 out of 100. The Journal of experimental medicine 2020-12-01

Variations in many genes linked to sporadic Alzheimer's disease (AD) show abundant expression in microglia, but relationships among these genes remain largely elusive. 4 key findings →

Evidence: low

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

Mitochondrial DNA variants observed in Alzheimer disease and Parkinson disease patients

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Genomics 1993-07-01

Mitochondrial DNA (mtDNA) variants associated with Alzheimer disease (AD) and Parkinson disease (PD) were sought by restriction endonuclease analysis in a cohort of 71 late-onset Caucasian patients. 4 key findings →

Evidence: moderate

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

15 years of longitudinal genetic, clinical, cognitive, imaging, and biochemical measures in DIAN

✓ Peer-reviewed alzhub usefulness score 50 out of 100. npj Dementia 2026-02-16

The Dominantly Inherited Alzheimer Network Observational Study (DIAN Obs) is a longitudinal, global cohort study investigating brain aging and autosomal dominant Alzheimer’s disease (ADAD), a rare monogenic form of Alzheimer’s disease (AD). 5 key findings →

Design: cohort study Evidence: moderate

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

The presenilin hypothesis of Alzheimer's disease: evidence for a loss-of-function pathogenic mechanism

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2006-12-29

Dominantly inherited mutations in the genes encoding presenilins (PS) and the amyloid precursor protein (APP) are the major causes of familial Alzheimer's disease (AD). 1 key finding →

Evidence: low

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

Translation of the alzheimer amyloid precursor protein mRNA is up-regulated by interleukin-1 through 5'-untranslated region sequences

✓ Peer-reviewed alzhub usefulness score 49 out of 100. The Journal of biological chemistry 1999-03-01

The amyloid precursor protein (APP) has been associated with Alzheimer's disease (AD) because APP is processed into the beta-peptide that accumulates in amyloid plaques, and APP gene mutations can cause early onset AD. 4 key findings →

Evidence: low

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

Microglia‐specific Alzheimer's disease polygenic risk score predicts longitudinal increase in plasma tau and faster cognitive decline in cognitively unimpaired older adults

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Alzheimer s & Dementia 2025-12-01

We included 1179 CU subjects (n = 474 females (40%), 70.9 ± 4.5 years old) of European descent who had pTau217 and PACC. 5 key findings →

Design: longitudinal study Participants: 474 Evidence: moderate

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

GWAS Identifies 44 Independent Associated Genomic Loci for Self-Reported Adult Hearing Difficulty in UK Biobank

✓ Peer-reviewed alzhub usefulness score 48 out of 100. American journal of human genetics 2019-09-26

Age-related hearing impairment (ARHI) is the most common sensory impairment in the aging population; a third of individuals are affected by disabling hearing loss by the age of 65. 3 key findings →

Evidence: low

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

Excessive production of amyloid beta-protein by peripheral cells of symptomatic and presymptomatic patients carrying the Swedish familial Alzheimer disease mutation

✓ Peer-reviewed alzhub usefulness score 48 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1994-12-01

The 39- to 43-amino acid amyloid beta-protein (A beta), which is progressively deposited in cerebral plaques and blood vessels in Alzheimer disease (AD), is secreted by cultured human cells during normal metabolism. 4 key findings →

Evidence: low

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

Interaction between amyloid precursor protein and presenilins in mammalian cells: implications for the pathogenesis of Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 48 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1997-07-01

Mutations in the presenilin 1 (PS1) and presenilin 2 (PS2) genes increase the production of the highly amyloidogenic 42-residue form of amyloid beta-protein (Abeta42) in a variety of cell lines and transgenic mice. 4 key findings →

Evidence: low

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

Reducing amyloid plaque burden via ex vivo gene delivery of an Abeta-degrading protease: a novel therapeutic approach to Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 48 out of 100. PLoS medicine 2007-08-01

Understanding the mechanisms of amyloid-beta protein (Abeta) production and clearance in the brain has been essential to elucidating the etiology of Alzheimer disease (AD). 4 key findings →

Evidence: low

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

Whole-genome sequencing reveals new Alzheimer's disease-associated rare variants in loci related to synaptic function and neuronal development

✓ Peer-reviewed alzhub usefulness score 48 out of 100. Alzheimer's & dementia : the journal of the Alzheimer's Association 2020-11-12

Genome-wide association studies have led to numerous genetic loci associated with Alzheimer's disease (AD). 2 key findings →

Participants: 2,247 Evidence: low

Full summary, score breakdown and related studies → Original source

Crucial role of calbindin-D28k in the pathogenesis of Alzheimer's disease mouse model

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Cell death and differentiation 2014-05-23

Calbindin-D28k (CB), one of the major calcium-binding and buffering proteins, has a critical role in preventing a neuronal death as well as maintaining calcium homeostasis. 4 key findings →

Evidence: low

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

Microglial function, INPP5D/SHIP1 signaling, and NLRP3 inflammasome activation: implications for Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Molecular neurodegeneration 2023-11-29

Recent genetic studies on Alzheimer's disease (AD) have brought microglia under the spotlight, as loci associated with AD risk are enriched in genes expressed in microglia. 4 key findings →

Evidence: low

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

TGF-β Pathway–Based Polygenic Risk Score Modifies the Association between Red Meat Intake and Colorectal Cancer Risk: Application of a Novel Pathway-Based PRS Method

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Cancer Epidemiology Biomarkers & Prevention 2026-04-01

A total of 30 variants were overrepresented in four pathways: presenilin/Alzheimer disease, cadherin/WNT signaling, gonadotropin-releasing hormone receptor, and transforming growth factor-β (TGF-β) signaling. 5 key findings →

Participants: 204 Evidence: low

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

Cognitive and neurobiologic markers of early Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 46 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1996-11-01

Recent studies indicate that impairments in two cognitive domains characterize the cognitive abnormalities that appear earliest in the course of Alzheimer disease (AD). 2 key findings →

Evidence: low

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

Comparative mapping of DNA markers from the familial Alzheimer disease and Down syndrome regions of human chromosome 21 to mouse chromosomes 16 and 17

✓ Peer-reviewed alzhub usefulness score 46 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1988-08-01

Mouse trisomy 16 has been proposed as an animal model of Down syndrome (DS), since this chromosome contains homologues of several loci from the q22 band of human chromosome 21. 1 key finding →

Evidence: low

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

Association between Hypothyroidism Onset and Alzheimer Disease Onset in Adults with Down Syndrome

✓ Peer-reviewed alzhub usefulness score 46 out of 100. Brain sciences 2021-09-16

Adults with Down syndrome (DS) have an exceptionally high frequency of Alzheimer disease (AD) with a wide variability in onset, from 40 to 70 years of age. 2 key findings →

Participants: 232 Evidence: low

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

DNA synthesis and neuronal apoptosis caused by familial Alzheimer disease mutants of the amyloid precursor protein are mediated by the p21 activated kinase PAK3

✓ Peer-reviewed alzhub usefulness score 46 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2003-07-01

Apoptotic pathways and DNA synthesis are activated in neurons in the brains of individuals with Alzheimer disease (AD). 4 key findings →

Evidence: low

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

Type 2 diabetes and late-onset Alzheimer’s disease and related dementia: A longitudinal cohort study integrating polygenic risk score

✓ Peer-reviewed alzhub usefulness score 46 out of 100. Journal of Alzheimer s Disease 2025-03-25

T2DM is one of the strong risk factors of ADRD but genetic T2DM effect does not contribute to ADRD risk. 3 key findings →

Evidence: moderate

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

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

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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 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