alzhub.org
Get help now — free helplines

You can call any of these for free. You do not need a diagnosis, an appointment, or a crisis to call — questions and plain exhaustion are reasons enough.

  • Alzheimer's Association 24/7 Helpline 800-272-3900 24 hours a day, 365 days a year Free, confidential support and information for people with dementia, caregivers, families and the public. Master's-level clinicians. Also Spanish.
  • 988 Suicide & Crisis Lifeline 988 24/7 Call or text 988, or chat at 988lifeline.org. For anyone in emotional distress or a mental-health crisis, including caregivers.
  • Alzheimer's Foundation of America (AFA) Helpline 866-232-8484 9:00 am - 9:00 pm ET, seven days a week Licensed social workers providing support, info and referrals. Also text message and web chat. Text: 646-586-5283

In a medical emergency, call 911. More numbers, and what each line does, on the help page.

Research

29,380 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 301–325 of 566 studies in Lewy body dementia (page 13 of 23) · 29,380 in the whole library · How the 0–100 score works

Download bibliography of the first 500 of these 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; 14,855 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.

Mechanistic View of hnRNPA2 Low-Complexity Domain Structure, Interactions, and Phase Separation Altered by Mutation and Arginine Methylation

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Molecular cell 2018-01-18

hnRNPA2, a component of RNA-processing membraneless organelles, forms inclusions when mutated in a syndrome characterized by the degeneration of neurons (bearing features of amyotrophic lateral sclerosis [ALS] and frontotemporal dementia), muscle, and bone. 1 key finding →

Evidence: low

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

The role of liquid-liquid phase separation in aggregation of the TDP-43 low-complexity domain

✓ Peer-reviewed alzhub usefulness score 50 out of 100. The Journal of biological chemistry 2019-02-27

Pathological aggregation of the transactive response DNA-binding protein of 43 kDa (TDP-43) is associated with several neurodegenerative disorders, including ALS, frontotemporal dementia, chronic traumatic encephalopathy, and Alzheimer's disease. 2 key findings →

Evidence: low

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

Gain and loss of function of ALS-related mutations of TARDBP (TDP-43) cause motor deficits in vivo

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Human molecular genetics 2009-12-03

TDP-43 has been found in inclusion bodies of multiple neurological disorders, including amyotrophic lateral sclerosis, frontotemporal dementia, Parkinson's disease and Alzheimer's disease. 1 key finding →

Evidence: low

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

MAPT mutations, tauopathy, and mechanisms of neurodegeneration

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Laboratory investigation; a journal of technical methods and pathology 2019-02-11

In multiple neurodegenerative diseases, including Alzheimer's disease (AD), a prominent pathological feature is the aberrant aggregation and inclusion formation of the microtubule-associated protein tau. 5 key findings →

Evidence: low

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

The touchscreen operant platform for testing learning and memory in rats and mice

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Nature protocols 2013-09-19

An increasingly popular method of assessing cognitive functions in rodents is the automated touchscreen platform, on which a number of different cognitive tests can be run in a manner very similar to touchscreen methods currently used to test human subjects. 5 key findings →

Evidence: low

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

Alzheimer disease with amygdala Lewy bodies: a distinct form of alpha-synucleinopathy

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Journal of neuropathology and experimental neurology 2006-07-01

Lewy bodies (LBs) are alpha-synuclein-immunoreactive neuronal inclusions with a predilection for specific cortical and subcortical regions, including the amygdala. 2 key findings →

Evidence: low

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

Colocalization of tau and alpha-synuclein epitopes in Lewy bodies

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Journal of neuropathology and experimental neurology 2003-04-01

The major protein constituent of Lewy bodies (LBs), the pathological hallmark of Parkinson disease and dementia with Lewy bodies, is considered to be alpha-synuclein, but other proteins, in particular the microtubule-associated protein tau, have been implicated in the pathogenesis of LBs. 2 key findings →

Evidence: low

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

Cerebrovascular dysfunction and microcirculation rarefaction precede white matter lesions in a mouse genetic model of cerebral ischemic small vessel disease

✓ Peer-reviewed alzhub usefulness score 50 out of 100. The Journal of clinical investigation 2010-01-11

Cerebral ischemic small vessel disease (SVD) is the leading cause of vascular dementia and a major contributor to stroke in humans. 5 key findings →

Evidence: low

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

Quantification of Lewy body pathology by cerebrospinal fluid endpoint dilution RT-QuIC in a neuropathological autopsy cohort of clinically heterogeneous participants

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Acta Neuropathologica 2025-06-23

The identification of biomarkers predicting the burden of brain alpha-synuclein (α-syn) pathology in vivo represents a research priority in Lewy body disease (LBD). 5 key findings →

Evidence: low

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

Elevated Cerebrospinal Fluid α‐Synuclein Seeding Activity Predicts Central Lewy Body Diseases

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Movement Disorders Clinical Practice 2025-01-16

Of 11 subjects with average AUCs above 500,000 units, 7 (64%) developed a central LBD compared to 1 of 20 (5%), with AUCs below the cutoff value (P = 0.0011 by log-rank test). 3 key findings →

Design: longitudinal study Evidence: moderate

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

Autonomic Dysfunction in Patients With Dementia With Lewy Bodies and Its Relationship With Nigrostriatal Denervation

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Neurology 2025-03-20

= 0.029). Despite the absence of overt nOH, patients with DLB show covert dysautonomia encompassing adrenergic, parasympathetic, and sudomotor dysfunction, highlighting the importance of standardized autonomic evaluation. 3 key findings →

Design: cohort study Evidence: moderate

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

Key motor and non-motor features in early dementia with Lewy bodies

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Frontiers in Neurology 2025-03-13

Early-stage DLB closely resembles PD in motor symptoms but has more neuropsychiatric non-motor symptoms compared to PD and overall non-motor symptoms than AD. 3 key findings →

Design: cross-sectional Participants: 107 Evidence: low

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

Tau pathology in Alzheimer disease and other tauopathies

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Biochimica et biophysica acta 2005-01-01

Just as neuronal activity is essential to normal brain function, microtubule-associated protein tau appears to be critical to normal neuronal activity in the mammalian brain, especially in the evolutionary most advanced species, the homo sapiens. 2 key findings →

Evidence: low

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

The neuropathology of traumatic brain injury

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Handbook of clinical neurology 2015-01-01

Traumatic brain injury, a leading cause of mortality and morbidity, is divided into three grades of severity: mild, moderate, and severe, based on the Glasgow Coma Scale, the loss of consciousness, and the development of post-traumatic amnesia. 3 key findings →

Evidence: low

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

Etiology and pathogenesis of Parkinson's disease

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Movement disorders : official journal of the Movement Disorder Society 2011-05-01

The past 25 years have seen a major expansion of knowledge concerning the cause of Parkinson's disease provided by an understanding of environmental and genetic factors that underlie the loss of nigral dopaminergic neurons. 5 key findings →

Evidence: low

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

↑ Change the filters

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 29,380 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 29,380 records, built mostly from automated pulls of Europe PMC (63.3% of the library) and OpenAlex (17.3%), 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.

1,037 records (3.5% of the library) are not peer-reviewed — 964 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