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Research

30,980 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 26–46 of 46 studies with an author at Indiana University Indianapolis (US) · tagged Genetics (page 2 of 2) · 30,980 in the whole library · How the 0–100 score works

Download bibliography of these 46 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; 16,452 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.

The Trem2 R47H variant confers loss-of-function-like phenotypes in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Molecular neurodegeneration 2018-06-01

The R47H variant of Triggering Receptor Expressed on Myeloid cells 2 (TREM2) confers greatly increased risk for Alzheimer's disease (AD), reflective of a central role for myeloid cells in neurodegeneration. 4 key findings →

Evidence: low

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

Convergent functional genomics of schizophrenia: from comprehensive understanding to genetic risk prediction

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Molecular psychiatry 2012-05-15

We have used a translational convergent functional genomics (CFG) approach to identify and prioritize genes involved in schizophrenia, by gene-level integration of genome-wide association study data with other genetic and gene expression studies in humans and animal models. 3 key findings →

Evidence: low

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

TREM2 deficiency exacerbates tau pathology through dysregulated kinase signaling in a mouse model of tauopathy

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Molecular neurodegeneration 2017-10-16

Here we report that TREM2 deficiency leads to accelerated and exacerbated hyperphosphorylation and aggregation of tau in a humanized mouse model of tauopathy. 4 key findings →

Evidence: low

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

Vascular variant of prion protein cerebral amyloidosis with tau-positive neurofibrillary tangles: the phenotype of the stop codon 145 mutation in PRNP

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1996-01-01

Deposition of PrP amyloid in cerebral vessels in conjunction with neurofibrillary lesions is the neuropathologic hallmark of the dementia associated with a stop mutation at codon 145 of PRNP, the gene encoding the prion protein (PrP). 4 key findings →

Evidence: low

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

SNPing away at complex diseases: analysis of single-nucleotide polymorphisms around APOE in Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 48 out of 100. American journal of human genetics 2000-06-21

There has been great interest in the prospects of using single-nucleotide polymorphisms (SNPs) in the search for complex disease genes, and several initiatives devoted to the identification and mapping of SNPs throughout the human genome are currently underway. 2 key findings →

Evidence: low

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

Genetic heterogeneity in Alzheimer disease and implications for treatment strategies

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Current neurology and neuroscience reports 2014-11-01

Since the original publication describing the illness in 1907, the genetic understanding of Alzheimer's disease (AD) has advanced such that it is now clear that it is a genetically heterogeneous condition, the subtypes of which may not uniformly respond to a given intervention. 5 key findings →

Evidence: low

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

Trem2 Y38C mutation and loss of Trem2 impairs neuronal synapses in adult mice

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Molecular neurodegeneration 2020-10-28

The Trem2 variant R47H, confers substantially elevated risk of developing late onset Alzheimer's disease, while NHD-linked Trem2 variants like Y38C, are associated with development of early onset dementia with white matter pathology. 4 key findings →

Evidence: low

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

MicroRNA-339-5p down-regulates protein expression of β-site amyloid precursor protein-cleaving enzyme 1 (BACE1) in human primary brain cultures and is reduced in brain tissue specimens of Alzheimer disease subjects

✓ Peer-reviewed alzhub usefulness score 44 out of 100. The Journal of biological chemistry 2013-12-18

Alzheimer disease (AD) results, in part, from the excess accumulation of the amyloid-β (Aβ) peptide as neuritic plaques in the brain. 4 key findings →

Evidence: low

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

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

IMAGING OF THE BONE ARCHITECTURE IN THE CONTEXT OF ALZHEIMER DISEASE

✓ Peer-reviewed alzhub usefulness score 42 out of 100. Osteoarthritis Imaging 2026-01-01

Female Psen1 mutation(L166P) mice were found to have reductions in whole-body mineral density (BMD) and bone mineral content as early as one month and a sustained bone phenotype with age with loss in cortical and trabecular properties compared to age-and gendermatched wildtype control mice, whereas male mice did not (Fig.1A-C). 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Cryo‐EM structures of amyloid β filaments from cotton wool plaques in Alzheimer disease caused by the PSEN1 V261I and A431E mutations

✓ Peer-reviewed alzhub usefulness score 31 out of 100. Alzheimer s & Dementia 2025-12-01

CWPs consist predominantly of two novel arrangements of type I Aβ filaments, and we have designated them as type Ic and type Id Aβ filaments. 5 key findings →

Evidence: low

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

Abnormalities in core AD biomarkers precede inflammatory and glial markers in CSF in Autosomal Dominant Alzheimer’s Disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-04-01

Increasing evidence suggests that accurate prediction of Alzheimer’s disease (AD) symptom onset requires more than amyloid- and tau-centric biomarkers such as cerebrospinal fluid (CSF) Aβ42/40, total tau and p-tau181 and plasma p-tau217. 4 key findings →

Participants: 484 Evidence: low

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

GCH1 genetic variation as a prognostic factor in Parkinsons disease across populations

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-08-19

BackgroundPathogenic variants in GCH1 have been associated with Parkinsons disease (PD), but the clinical phenotype and longitudinal disease course of GCH1-associated PD remain incompletely characterized. 5 key findings →

Design: longitudinal study Participants: 22,825 Evidence: moderate

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 30,980 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 30,980 records, built mostly from automated pulls of Europe PMC (65.2% of the library) and OpenAlex (16.4%), 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.

1,042 records (3.4% of the library) are not peer-reviewed — 967 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