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Research

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

Find studies

Showing 326–350 of 566 studies in Lewy body dementia (page 14 of 23) · 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 “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.

Physical activity, APOE genotype, and dementia risk: findings from the Cardiovascular Health Cognition Study

✓ Peer-reviewed alzhub usefulness score 49 out of 100. American journal of epidemiology 2005-04-01

Physical activity may help preserve cognitive function and decrease dementia risk, but epidemiologic findings are inconsistent. 1 key finding →

Evidence: low

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

Inhibition of heparin-induced tau filament formation by phenothiazines, polyphenols, and porphyrins

✓ Peer-reviewed alzhub usefulness score 49 out of 100. The Journal of biological chemistry 2004-12-17

Tau protein is the major component of the intraneuronal filamentous inclusions that constitute defining neuropathological characteristics of Alzheimer's disease and other tauopathies. 1 key finding →

Evidence: low

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

TAR DNA-binding protein 43 in neurodegenerative disease

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Nature reviews. Neurology 2010-03-16

In 2006, TAR DNA-binding protein 43 (TDP-43), a highly conserved nuclear protein, was identified as the major disease protein in amyotrophic lateral sclerosis (ALS) and in the most common variant of frontotemporal lobar degeneration (FTLD), FTLD-U, which is characterized by cytoplasmic inclusions that stain positive for ubiquitin but negative for tau and alpha-synuclein. 5 key findings →

Evidence: low

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

Accumulation of pathological tau species and memory loss in a conditional model of tauopathy

✓ Peer-reviewed alzhub usefulness score 49 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2007-04-01

Neurofibrillary tangles (NFTs) are a pathological hallmark of Alzheimer's disease and other tauopathies, but recent studies in a conditional mouse model of tauopathy (rTg4510) have suggested that NFT formation can be dissociated from memory loss and neurodegeneration. 3 key findings →

Evidence: low

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

Proteomic and functional analyses reveal a mitochondrial dysfunction in P301L tau transgenic mice

✓ Peer-reviewed alzhub usefulness score 49 out of 100. The Journal of biological chemistry 2005-04-14

Transgenic mice overexpressing the P301L mutant human tau protein exhibit an accumulation of hyperphosphorylated tau and develop neurofibrillary tangles. 5 key findings →

Evidence: low

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

Mechanisms of Parkinson's disease linked to pathological alpha-synuclein: new targets for drug discovery

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Neuron 2006-10-01

Classic Parkinson's disease (PD) is characterized by fibrillar alpha-synuclein inclusions known as Lewy bodies in the substantia nigra, which are associated with nigrostriatal degeneration. 1 key finding →

Evidence: low

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

Tau proteins with FTDP-17 mutations have a reduced ability to promote microtubule assembly

✓ Peer-reviewed alzhub usefulness score 49 out of 100. FEBS letters 1998-10-01

Recently exonic and intronic mutations in the gene for microtubule-associated protein tau have been discovered in cases of familial frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17). 5 key findings →

Evidence: low

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

Oxidative stress as a cause of nigral cell death in Parkinson's disease and incidental Lewy body disease. The Royal Kings and Queens Parkinson's Disease Research Group

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Annals of neurology 1992-01-01

We examine the evidence for free radical involvement and oxidative stress in the pathological process underlying Parkinson's disease, from postmortem brain tissue. 4 key findings →

Evidence: low

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

Physiological functions and pathobiology of TDP-43 and FUS/TLS proteins

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Journal of neurochemistry 2016-06-15

The multiple roles played by RNA binding proteins in neurodegeneration have become apparent following the discovery of TAR DNA binding protein 43 kDa (TDP-43) and fused in sarcoma/translocated in liposarcoma (FUS/TLS) involvement in amyotrophic lateral sclerosis and frontotemporal lobar dementia. 5 key findings →

Evidence: low

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

Source-based morphometry: the use of independent component analysis to identify gray matter differences with application to schizophrenia

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Human brain mapping 2009-03-01

We present a multivariate alternative to the voxel-based morphometry (VBM) approach called source-based morphometry (SBM), to study gray matter differences between patients and healthy controls. 4 key findings →

Evidence: low

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

The two faces of protein misfolding: gain- and loss-of-function in neurodegenerative diseases

✓ Peer-reviewed alzhub usefulness score 49 out of 100. The EMBO journal 2008-01-01

The etiologies of neurodegenerative diseases may be diverse; however, a common pathological denominator is the formation of aberrant protein conformers and the occurrence of pathognomonic proteinaceous deposits. 1 key finding →

Evidence: low

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

Multi-modal comparative phenotyping of knock-in mouse models of frontotemporal dementia/amyotrophic lateral sclerosis

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Disease Models & Mechanisms 2025-08-01

Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are progressive adult-onset neurodegenerative diseases with overlapping pathological and genetic origins. 3 key findings →

Design: longitudinal study Evidence: moderate

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 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