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Research

31,780 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 101–120 of 120 studies in Lewy body dementia · tagged Genetics (page 5 of 5) · 31,780 in the whole library · How the 0–100 score works

Download bibliography of these 120 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.

Other subjects

Authors

Names as each record prints them; the same person can appear under two spellings.

Institutions

From OpenAlex; 17,251 studies have no institution on record and are not counted here.

What “Lewy body dementia” covers

Lewy body dementia — Dementia with Lewy bodies and related conditions: how they differ from Alzheimer's in symptoms, diagnosis and care.

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.

Mitochondrial dysfunction associated with increased oxidative stress and α-synuclein accumulation in PARK2 iPSC-derived neurons and postmortem brain tissue

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Molecular brain 2012-10-06

Pathogenic changes in the brain of a PARK2 patient were recapitulated using iPSC technology. 1 key finding →

Evidence: low

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

alpha-synuclein fibrillogenesis is nucleation-dependent. Implications for the pathogenesis of Parkinson's disease

✓ Peer-reviewed alzhub usefulness score 45 out of 100. The Journal of biological chemistry 1999-07-01

Parkinson's disease (PD) is a neurodegenerative disorder that is pathologically characterized by the presence of intracytoplasmic Lewy bodies, the major components of which are filaments consisting of alpha-synuclein. 1 key finding →

Evidence: low

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

Transgenic mice carrying a human mutant superoxide dismutase transgene develop neuronal cytoskeletal pathology resembling human amyotrophic lateral sclerosis lesions

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1996-04-01

Mutations in the human Cu,Zn superoxide dismutase gene (SOD1) are found in 20% of kindreds with familial amyotrophic lateral sclerosis. 3 key findings →

Evidence: low

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

Amyotrophic lateral sclerosis and frontotemporal dementia mutation reduces endothelial TDP-43 and causes blood-brain barrier defects

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Science Advances 2025-04-16

Mutations in the TARDBP gene encoding TDP-43 protein are linked to loss of function in neurons and familial frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS). 5 key findings →

Evidence: low

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

Structural and functional connectivity in tau mutation carriers: from presymptomatic to symptomatic frontotemporal dementia

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Alzheimer s & Dementia 2025-07-01

Early isolated functional disruptions in salience/visual networks were present in asymptomatic carriers, along with anterior cingulate gray matter reductions. 5 key findings →

Evidence: low

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

Reasons for and against presymptomatic genetic testing in frontotemporal dementia: a qualitative study

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Human Genetics 2026-02-16

The majority of individuals at 50% risk of carrying a pathogenic variant causing frontotemporal dementia (FTD) chooses not to undergo presymptomatic genetic testing. 5 key findings →

Participants: 14 Evidence: low

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

Genome‐wide association analysis identifies APOE as a mitophagy modifier in Lewy body disease

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Alzheimer s & Dementia 2025-04-01

We identified a significant genome-wide association with p-S65-Ub for rs429358 (apolipoprotein E ε4 [APOE4]) and a suggestive association for rs6480922 (ZMIZ1). 5 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

The experience of “at‐risk” status for familial frontotemporal dementia (fFTD) and its impact on reproductive decision‐making: A qualitative study

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Journal of Genetic Counseling 2025-01-12

Familial frontotemporal dementia (fFTD) is an autosomal dominant heritable form of FTD, onsetting in mid-life, characterized by behavioral and personality changes. 5 key findings →

Evidence: low

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

Frontotemporal dementia as a consequence of GRN mutations: From disease cause to models to therapies

✓ Peer-reviewed alzhub usefulness score 39 out of 100. Pharmacological Research 2025-09-17

Frontotemporal dementia (FTD) encompasses a broad, clinically and neuropathologically diverse group of neurodegenerative disorders associated with changes in personality, behaviour, and/or language due to the progressive degeneration of the frontal and temporal lobes of the brain. 3 key findings →

Evidence: low

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

Ethics of disclosure of onset‐predictive biomarker test results for genetic frontotemporal dementia in the research context

✓ Peer-reviewed alzhub usefulness score 39 out of 100. Alzheimer s & Dementia Diagnosis Assessment & Disease Monitoring 2025-04-01

Onset-predictive biomarker tests (OPBTs) for genetic frontotemporal dementia (FTD) may predict symptom onset in coming years. 4 key findings →

Evidence: low

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

Novel approaches for the treatment of frontotemporal dementia: is there hope for the future?

✓ Peer-reviewed alzhub usefulness score 38 out of 100. Expert Review of Neurotherapeutics 2025-08-13

Frontotemporal dementia (FTD) refers to a group of neurodegenerative disorders characterized clinically by behavioral disturbances and pathologically by frontal and anterior temporal lobe neurodegeneration, resulting in brain atrophy. 5 key findings →

Evidence: high

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

Preclinical and Prodromal Frontotemporal Dementia: Challenges and Opportunities

✓ Peer-reviewed alzhub usefulness score 34 out of 100. International Journal of Translational Medicine 2025-11-15

Frontotemporal lobar degeneration (FTLD) represents a heterogeneous group of neurodegenerative disorders with overlapping clinical, pathological, and genetic characteristics. 1 key finding →

Evidence: low

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

Endocannabinoid System Genes in Dementia: A Systematic Mendelian Randomization Study of Functional Variants and Tissue-Specific Expression Across Clinical, Molecular, and Neuroimaging Phenotypes

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

ResultsThe CNR2 missense variant rs4649124 was associated with increased vascular dementia risk (BH-adjusted P = 0.049) after correction at the 5% false discovery rate (FDR) threshold, with additional associations at the 10% FDR threshold for all-cause dementia risk (BH-adjusted P = 0.051) and lower circulating APP (BH-adjusted P = 0.088) and BDNF (BH-adjusted P = 0.083) levels. 5 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
  • 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 31,780 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 31,780 records, built mostly from automated pulls of Europe PMC (66% of the library) and OpenAlex (16%), 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.

1,052 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