Lewy body dementia: research in the library

• 566studies on this subject, of 27,380 in the library
• 547peer-reviewed
• 1967–2026years published
• 51median usefulness score out of 100

These counts and lists are worked out from the library itself each time the page loads. A score rates how much weight a study can bear — its design, journal, evidence and recency — not whether its result is good news. How we score a study.

1. A multicentre validation study of the diagnostic value of plasma neurofilament light Nature communications · 2021-06-07 · usefulness score 71/100 · Peer-reviewed
   • Biomarkers
   • Other Dementias

   Across 2,269 people in two cohorts (King's College London and Sweden's BioFINDER), a blood marker of nerve-cell damage, plasma neurofilament light (NfL), was raised in all cortical neurodegenerative disorders, ALS and atypical parkinsonian disorders. That means a high level signals neurodegeneration in general, not Alzheimer's in particular. The authors found it useful for specific questions, such as spotting dementia in people with Down syndrome or separating dementia from psychiatric illness, and found it worked best for ruling out neurodegeneration, provided age-appropriate cut-offs are used. It is a diagnostic test study and does not treat or prevent any of these conditions.

2. A clinico-pathological study of subtypes in Parkinson's disease Brain : a journal of neurology · 2009-09-16 · usefulness score 69/100 · Peer-reviewed
   • Other Dementias
   • Brain Biology

   This study of Parkinson's disease subtypes found that a non-tremor dominant pattern was strongly associated with cognitive disability and more cortical Lewy bodies and amyloid-beta plaque load. It does not test any treatment or prevention for Alzheimer's disease, so it has no direct implications for treating, curing, or preventing the disease.

3. Comparison of risperidone and placebo for psychosis and behavioral disturbances associated with dementia: a randomized, double-blind trial. Risperidone Study Group The Journal of clinical psychiatry · 1999-02-01 · usefulness score 68/100 · Peer-reviewed
   • Clinical Trials
   • Other Dementias

   In this 12-week trial of 625 patients with severe dementia, risperidone at 1 and 2 mg/day reduced psychosis and aggression scores more than placebo. It treats behavioral symptoms only and does not affect the underlying disease or its progression.

4. Blood-brain barrier: ageing and microvascular disease--systematic review and meta-analysis Neurobiology of aging · 2007-09-14 · usefulness score 66/100 · Peer-reviewed
   • Brain Biology

   This systematic review and meta-analysis found that the blood-brain barrier becomes more permeable with normal ageing and even more so in people with vascular or Alzheimer's dementia. It suggests that increased blood-brain barrier permeability may be an important mechanism in the beginning or worsening of cerebral microvascular disease, but further studies are needed and no treatment is tested.

5. Neurodegenerative disease concomitant proteinopathies are prevalent, age-related and APOE4-associated Brain : a journal of neurology · 2018-07-01 · usefulness score 66/100 · Peer-reviewed
   • Other Dementias

   This study reports that, in neurodegenerative diseases, brains often carry more than one type of abnormal protein build-up ("concomitant proteinopathies"), that this becomes more common with age, and that it is linked to the APOE ɛ4 gene variant; the APOE ɛ4 link is stated specifically for ALS and neocortical Lewy body disease. The authors say this matters for clinical trials of single-target treatments aimed at tau, amyloid-β, α-synuclein or TDP-43. The record gives no prevalence figures or effect sizes, and an association with APOE ɛ4 does not show that the gene causes these build-ups.

6. Identifying dementia outcomes in UK Biobank: a validation study of primary care, hospital admissions and mortality data European journal of epidemiology · 2019-02-26 · usefulness score 66/100 · Peer-reviewed
   • Care Services

   This validation study checked how accurately dementia diagnoses in UK Biobank primary care, hospital and mortality records matched expert review of medical records, finding positive predictive values of roughly 50% to 87% depending on the dataset and dementia type. It is about identifying dementia cases for research, not about treatment, cure or prevention.

7. Novel mutations in TARDBP (TDP-43) in patients with familial amyotrophic lateral sclerosis PLoS genetics · 2008-09-19 · usefulness score 65/100 · Peer-reviewed
   • Genetics
   • Other Dementias
   • Brain Biology

   In a screen of 296 patients with TDP-43-related brain diseases, three TARDBP gene changes turned up only in familial ALS (3 of 92, 3.3%), not in 24 sporadic ALS or 180 other TDP-43 disease patients, and were absent from 825 controls. Patient cell lines showed more caspase-cleaved TDP-43 fragments than controls, which the authors say "support TARDBP mutations as a cause of ALS"; the mechanism they propose is stated as speculation. This is ALS genetics, not a finding about Alzheimer's disease, and it tests no treatment.

8. The effect of Lewy body (co-)pathology on the clinical and imaging phenotype of amnestic patients Brain · 2025-01-31 · usefulness score 65/100 · Peer-reviewed
   • Brain Scans
   • Other Dementias

   Lewy body co-pathology in Alzheimer's disease was associated with more severe hypometabolism and faster cognitive decline, but did not affect the regional hypometabolic pattern or cognitive profile. These findings indicate the presence of Lewy body pathology may have different consequences depending on Alzheimer's disease co-morbidity, with implications for accurate diagnosis.

9. Association of missense and 5'-splice-site mutations in tau with the inherited dementia FTDP-17 Nature · 1998-06-01 · usefulness score 64/100 · Peer-reviewed
   • Genetics
   • Other Dementias

   This study identified missense and splice-site mutations in the tau gene in families with the inherited dementia FTDP-17. It concerns the genetic cause of that inherited dementia and does not test any treatment, cure or prevention for Alzheimer's disease.

10. National Institute on Aging-Alzheimer's Association guidelines for the neuropathologic assessment of Alzheimer's disease: a practical approach Acta neuropathologica · 2011-11-20 · usefulness score 64/100 · Peer-reviewed
    • Brain Biology

    These guidelines give a practical way to assess Alzheimer's brain changes in examined brain tissue, using an "ABC" score that combines amyloid β deposits (A), the stage of neurofibrillary tangles (B) and neuritic plaques (C), along with recommendations on brain sampling, staining and reporting. They also recognise that Alzheimer's brain changes "may occur in the apparent absence of cognitive impairment", and they set out more detailed ways to record common co-existing conditions such as Lewy body disease, vascular brain injury, hippocampal sclerosis and TDP-43 inclusions. This is a standard for examining brain tissue, not a test for living patients or a treatment.

11. Null mutations in progranulin cause ubiquitin-positive frontotemporal dementia linked to chromosome 17q21 Nature · 2006-07-16 · usefulness score 64/100 · Peer-reviewed
    • Other Dementias
    • Genetics

    This study found that mutations in the progranulin gene (PGRN) cause frontotemporal dementia linked to chromosome 17q21, with loss of the mutant allele and reduced PGRN expression. It provides genetic evidence that reduced PGRN-mediated neuronal survival leads to neurodegeneration, but no treatment was tested.

12. Diagnostic value of plasma phosphorylated tau181 in Alzheimer's disease and frontotemporal lobar degeneration Nature medicine · 2020-03-02 · usefulness score 64/100 · Peer-reviewed
    • Other Dementias
    • Diagnosis
    • Treatments

    In this 2020 study, levels of a blood protein, plasma pTau181, were 3.5 times higher in people with Alzheimer's disease than in controls. The test separated Alzheimer's from frontotemporal lobar degeneration with an area under the curve of 0.894 against clinically diagnosed cases and 0.878 against autopsy-confirmed cases, and it also identified people who were amyloid-PET-positive and correlated with tau-PET. The authors propose it as a cheaper, less invasive screen to decide which people with cognitive or behavioural symptoms should go on to fuller testing, not as a stand-alone diagnosis. The record does not report sample sizes, cut-offs or limitations.

13. TDP-43 represses cryptic exon inclusion in the FTD-ALS gene UNC13A Nature · 2022-02-23 · usefulness score 64/100 · Peer-reviewed
    • Genetics
    • Other Dementias
    • Brain Biology

    UNC13A gene variants are among the strongest genetic risk signals for FTD and ALS, but how they raise risk was unknown. In human brain tissue, neuronal cell lines and stem-cell-derived motor neurons, this study found that losing the protein TDP-43 from the nucleus lets a "cryptic exon" into UNC13A's RNA and lowers UNC13A protein, and that the top risk variants, located next to that exon, increase this mis-splicing when TDP-43 is not working. It is lab evidence linking a genetic risk factor to TDP-43 loss in FTD and ALS. It does not study Alzheimer's disease and tests no treatment.

14. TDP-43 loss and ALS-risk SNPs drive mis-splicing and depletion of UNC13A Nature · 2022-02-23 · usefulness score 64/100 · Peer-reviewed
    • Other Dementias
    • Brain Biology

    TDP-43 depletion causes a cryptic exon to be included in UNC13A, leading to loss of UNC13A protein, and common risk variants overlap with TDP-43 binding sites and worsen this. The authors call this a promising therapeutic target, but no treatment has been tested.

15. Genome sequencing analysis identifies new loci associated with Lewy body dementia and provides insights into its genetic architecture Nature genetics · 2021-02-15 · usefulness score 64/100 · Peer-reviewed
    • Genetics
    • Other Dementias

    Whole-genome sequencing in large cohorts identified five risk loci for Lewy body dementia and implicated mutations in the gene GBA, and genetic risk scores showed shared risk with Alzheimer's and Parkinson's diseases. This improves understanding of the genetic architecture of Lewy body dementia but reports no treatment or cure.

16. Neural language networks at birth Proceedings of the National Academy of Sciences of the United States of America · 2011-09-06 · usefulness score 64/100 · Peer-reviewed

    This study looked at brain activity in 2-day-old infants and found that language-related brain regions respond to speech at birth, but the connections within each hemisphere are still immature. It does not test any treatment or prevention for Alzheimer's disease, so it has no direct implications for treating, curing, or preventing the disease.

17. Genome-wide association meta-analysis of neuropathologic features of Alzheimer's disease and related dementias PLoS genetics · 2014-09-04 · usefulness score 64/100 · Peer-reviewed
    • Genetics
    • Brain Biology

    Using autopsy findings from 4,914 brains rather than clinical diagnoses, this genetic study linked APOE variants to plaques, tangles, amyloid in blood vessels and Lewy body disease, and found new associations for plaque burden (GALNT7, ABCG1, a chromosome 9 region) and hippocampal sclerosis (KCNMB2). It confirmed 12 of 21 known non-APOE Alzheimer's risk genes, 9 of them with larger odds ratios than in clinically diagnosed samples. These are statistical associations that point to biology worth studying; they do not test any treatment or predict an individual's risk.

18. A hexanucleotide repeat expansion in C9ORF72 is the cause of chromosome 9p21-linked ALS-FTD Neuron · 2011-09-21 · usefulness score 63/100 · Peer-reviewed
    • Other Dementias
    • Genetics

    This 2011 genetic study identified a large GGGGCC repeat expansion in the C9ORF72 gene as the cause of ALS and frontotemporal dementia linked to chromosome 9p21. In Finland it accounted for 46.0% of familial and 21.1% of sporadic ALS, and it was found in one-third of familial ALS cases of European descent, which the authors called the most common genetic cause of these diseases identified to date. The study concerns ALS and FTD, not Alzheimer's disease, gives no FTD-only figures, and does not test any treatment.

19. National Institute on Aging-Alzheimer's Association guidelines for the neuropathologic assessment of Alzheimer's disease Alzheimer's & dementia : the journal of the Alzheimer's Association · 2012-01-01 · usefulness score 63/100 · Peer-reviewed
    • Brain Biology

    A US–European consensus panel revised the 1997 guidelines for examining the brain after death for Alzheimer's disease. The update recognises a "pre-clinical stage" of the disease and assesses amyloid build-up as well as neurofibrillary change and neuritic plaques. It also sets protocols for Lewy body disease, vascular brain injury, hippocampal sclerosis and TDP-43 inclusions, and recommends standard ways to compare brain findings with a person's symptoms in life. These are standards for pathologists and researchers, not a test, treatment or prevention.

20. LRP1 is a master regulator of tau uptake and spread Nature · 2020-04-01 · usefulness score 63/100 · Peer-reviewed
    • Other Dementias
    • Brain Biology

    In cells and a mouse model, reducing LRP1 lowered tau uptake and spread between neurons, identifying LRP1 as a possible target for diseases involving tau spread. This is laboratory and animal work and does not yet show benefit in people.

See all 566 studies in Lewy body dementia, with filters →

• Frequency-Resolved Connectivity Graphs for EEG-Based Classification of Alzheimer and Frontotemporal Dementia bioRxiv · 2026-10-22 · usefulness score 16/100 · Preprint — not yet peer-reviewed
  • Other Dementias
• Dementia and PDE5 inhibitors: A retrospective cohort study of veterans Research Square · 2026-10-13 · usefulness score 16/100 · Preprint — not yet peer-reviewed
  • Other Dementias
• Decoding Dementia from Sweat: A Proof-of-Concept Label-Free Raman Fingerprinting of EVs medRxiv · 2026-10-01 · usefulness score 16/100 · Preprint — not yet peer-reviewed
• Phenome-wide and proteomic analysis of APOE alleles across different ancestries in the All of Us Research Program medRxiv · 2026-09-28 · usefulness score 16/100 · Preprint — not yet peer-reviewed
  • Genetics
  • Other Dementias
• DNA Methylation Concordance Between Fresh-Frozen and Formalin-Fixed Paraffin-Embedded Human Brain Tissue in Neurodegenerative Diseases Preprints.org · 2026-09-24 · usefulness score 16/100 · Preprint — not yet peer-reviewed
  • Other Dementias
• The value of a family history to distinguish monogenic from polygenic amyotrophic lateral sclerosis medRxiv (preprint) · 2026-09-22 · usefulness score 16/100 · Preprint — not yet peer-reviewed
  • Other Dementias
  • Genetics
• Underlying histopathology features of white matter hyperintensities in vascular and neurodegenerative disorders: a systematic review Research Square · 2026-09-20 · usefulness score 16/100 · Preprint — not yet peer-reviewed
  • Brain Scans
  • Other Dementias
  • Brain Biology
• Loss of TDP-43 function drives cryptic circular RNAs in neurodegenerative diseases bioRxiv · 2026-09-20 · usefulness score 16/100 · Preprint — not yet peer-reviewed
  • Brain Biology
  • Other Dementias
• Distinguishing Parkinsonian Disorders and Cognitive Disorder Subtypes Using Pseudocontinuous Arterial Spin Labeling Preprints.org · 2026-09-16 · usefulness score 16/100 · Preprint — not yet peer-reviewed
  • Other Dementias
• Diagnostic Value of Large Language Model-Extracted Gross Brain Findings in Neurodegenerative Diseases medRxiv (preprint) · 2026-09-14 · usefulness score 16/100 · Preprint — not yet peer-reviewed
  • Other Dementias
  • Diagnosis

All 566 studies in Lewy body dementia, newest first →

Studies by year published

Counts the 566 studies with a usable publication date. The library is a large sample of published work, not a complete index, so these counts describe the library, not the whole field.

• Getting a diagnosis
• Biomarkers
• Clinical trials
• Prevention and risk
• Caregiving
• How common it is
• Costs and economics
• Genetics
• Laboratory science
• Disease mechanisms
• Vascular contributions
• Prevention trials
• Clinical safety
• Health systems and care delivery
• End-of-life care
• Risk factors
• Digital health tools
• Treatments
• Disparities
• Mild cognitive impairment
• Risk genes beyond APOE
• Brain scans and imaging
• TREM2 and immune genetics
• Cognitive tests and assessment
• Down syndrome and Alzheimer's
• Long-term cohort studies
• Inflammation and the immune system
• Tau biomarkers
• Brain tissue and pathology
• Drug development
• Hippocampus size on brain scans

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