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Research

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

Find studies

Showing 1–25 of 60 studies in Lewy body dementia with an author at University of Pennsylvania (US) (page 1 of 3) · 31,780 in the whole library · How the 0–100 score works

Download bibliography of these 60 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.

Other 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.

Comparison of risperidone and placebo for psychosis and behavioral disturbances associated with dementia: a randomized, double-blind trial. Risperidone Study Group

✓ Peer-reviewed alzhub usefulness score 68 out of 100. The Journal of clinical psychiatry 1999-02-01

The study was completed by 70% of the patients. 4 key findings →

Participants: 625 Evidence: low

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

Association of missense and 5'-splice-site mutations in tau with the inherited dementia FTDP-17

✓ Peer-reviewed alzhub usefulness score 64 out of 100. Nature 1998-06-01

Thirteen families have been described with an autosomal dominantly inherited dementia named frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17), historically termed Pick's disease. 5 key findings →

Evidence: low

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

National Institute on Aging-Alzheimer's Association guidelines for the neuropathologic assessment of Alzheimer's disease: a practical approach

✓ Peer-reviewed alzhub usefulness score 64 out of 100. Acta neuropathologica 2011-11-20

We present a practical guide for the implementation of recently revised National Institute on Aging-Alzheimer's Association guidelines for the neuropathologic assessment of Alzheimer's disease (AD). 1 key finding →

Evidence: low

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

TDP-43 represses cryptic exon inclusion in the FTD-ALS gene UNC13A

✓ Peer-reviewed alzhub usefulness score 64 out of 100. Nature 2022-02-23

A hallmark pathological feature of the neurodegenerative diseases amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) is the depletion of RNA-binding protein TDP-43 from the nucleus of neurons in the brain and spinal cord 1 . 2 key findings →

Evidence: low

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

TDP-43 loss and ALS-risk SNPs drive mis-splicing and depletion of UNC13A

✓ Peer-reviewed alzhub usefulness score 64 out of 100. Nature 2022-02-23

Variants of UNC13A, a critical gene for synapse function, increase the risk of amyotrophic lateral sclerosis and frontotemporal dementia 1-3 , two related neurodegenerative diseases defined by mislocalization of the RNA-binding protein TDP-43 4,5 . 2 key findings →

Evidence: low

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

Genome-wide association meta-analysis of neuropathologic features of Alzheimer's disease and related dementias

✓ Peer-reviewed alzhub usefulness score 64 out of 100. PLoS genetics 2014-09-04

Alzheimer's disease (AD) and related dementias are a major public health challenge and present a therapeutic imperative for which we need additional insight into molecular pathogenesis. 2 key findings →

Evidence: low

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

National Institute on Aging-Alzheimer's Association guidelines for the neuropathologic assessment of Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 63 out of 100. Alzheimer's & dementia : the journal of the Alzheimer's Association 2012-01-01

A consensus panel from the United States and Europe was convened recently to update and revise the 1997 consensus guidelines for the neuropathologic evaluation of Alzheimer's disease (AD) and other diseases of brain that are common in the elderly. 2 key findings →

Evidence: low

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

Sex differences in the clinical manifestation of autosomal dominant frontotemporal dementia

✓ Peer-reviewed alzhub usefulness score 63 out of 100. Alzheimer s & Dementia 2025-04-01

While sex differences were not apparent at asymptomatic stages, females showed more rapid declines across all outcomes in symptomatic stages compared to males. 5 key findings →

Design: longitudinal study Participants: 337 Evidence: moderate

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

Ubiquitinated TDP-43 in frontotemporal lobar degeneration and amyotrophic lateral sclerosis

✓ Peer-reviewed alzhub usefulness score 62 out of 100. Science (New York, N.Y.) 2006-10-01

Ubiquitin-positive, tau- and alpha-synuclein-negative inclusions are hallmarks of frontotemporal lobar degeneration with ubiquitin-positive inclusions and amyotrophic lateral sclerosis. 1 key finding →

Evidence: low

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

Symmetric diffeomorphic image registration with cross-correlation: evaluating automated labeling of elderly and neurodegenerative brain

✓ Peer-reviewed alzhub usefulness score 61 out of 100. Medical image analysis 2007-06-23

One of the most challenging problems in modern neuroimaging is detailed characterization of neurodegeneration. 1 key finding →

Design: longitudinal study Evidence: moderate

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

TARDBP mutations in amyotrophic lateral sclerosis with TDP-43 neuropathology: a genetic and histopathological analysis

✓ Peer-reviewed alzhub usefulness score 61 out of 100. The Lancet. Neurology 2008-04-07

We identified two variants in TARDBP, which would encode Gly290Ala and Gly298Ser forms of TDP-43, in two kindreds with familial ALS. 2 key findings →

Participants: 259 Evidence: low

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

Cellular milieu imparts distinct pathological α-synuclein strains in α-synucleinopathies

✓ Peer-reviewed alzhub usefulness score 60 out of 100. Nature 2018-05-09

In Lewy body diseases-including Parkinson's disease, without or with dementia, dementia with Lewy bodies, and Alzheimer's disease with Lewy body co-pathology 1 -α-synuclein (α-Syn) aggregates in neurons as Lewy bodies and Lewy neurites 2 . 2 key findings →

Evidence: low

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

Oxidative damage linked to neurodegeneration by selective alpha-synuclein nitration in synucleinopathy lesions

✓ Peer-reviewed alzhub usefulness score 59 out of 100. Science (New York, N.Y.) 2000-11-01

Aggregated alpha-synuclein proteins form brain lesions that are hallmarks of neurodegenerative synucleinopathies, and oxidative stress has been implicated in the pathogenesis of some of these disorders. 4 key findings →

Evidence: low

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

Mutation-specific functional impairments in distinct tau isoforms of hereditary FTDP-17

✓ Peer-reviewed alzhub usefulness score 59 out of 100. Science (New York, N.Y.) 1998-12-01

Tau proteins aggregate as cytoplasmic inclusions in a number of neurodegenerative diseases, including Alzheimer's disease and hereditary frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17). 1 key finding →

Participants: 17 Evidence: low

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

TDP-43 in familial and sporadic frontotemporal lobar degeneration with ubiquitin inclusions

✓ Peer-reviewed alzhub usefulness score 59 out of 100. The American journal of pathology 2007-07-01

TAR DNA-binding protein 43 (TDP-43) is a major pathological protein of sporadic and familial frontotemporal lobar degeneration with ubiquitin-positive, tau-negative inclusions (FTLD-U) with or without motor neuron disease (MND). 1 key finding →

Participants: 36 Evidence: low

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

Exogenous α-synuclein fibrils induce Lewy body pathology leading to synaptic dysfunction and neuron death

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Neuron 2011-10-01

Inclusions composed of α-synuclein (α-syn), i.e., Lewy bodies (LBs) and Lewy neurites (LNs), define synucleinopathies including Parkinson's disease (PD) and dementia with Lewy bodies (DLB). 5 key findings →

Evidence: low

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

Cytoplasmic TDP-43 De-mixing Independent of Stress Granules Drives Inhibition of Nuclear Import, Loss of Nuclear TDP-43, and Cell Death

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Neuron 2019-03-07

While cytoplasmic aggregation of TDP-43 is a pathological hallmark of amyotrophic lateral sclerosis and frontotemporal dementia, how aggregates form and what drives its nuclear clearance have not been determined. 1 key finding →

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 31,780 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