Results 111 to 120 of about 8,460,931 (324)

Clinical prevalence of Lewy body dementia

Alzheimer's Research & Therapy, 2018
The prevalence of dementia with Lewy bodies (DLB) and dementia in Parkinson’s disease (PDD) in routine clinical practice is unclear. Prevalence rates observed in clinical and population-based cohorts and neuropathological studies vary greatly.
J. Kane, A. Surendranathan, A. Bentley, S. Barker, John-Paul Taylor, Alan J. Thomas, L. Allan, R. McNally, Peter W. James, I. McKeith, D. Burn, J. O'Brien   +11 more
semanticscholar   +1 more source

Sex differences for regional pathology in people with a high likelihood of Lewy body dementia phenotype based on underlying pathology

Alzheimer’s & Dementia: Diagnosis, Assessment & Disease Monitoring
Introduction Clinicopathological correlations differ by sex in Lewy body dementia (LBD). However, previous studies have focused on pathological staging systems that place less emphasis on regional pathologies.
Ece Bayram, David G. Coughlin, Shunsuke Koga, Owen A. Ross, Irene Litvan, Dennis W. Dickson   +5 more
doaj   +1 more source

Neuroimaging in Lewy body dementia

Journal of Neurology, 2018
Lewy body dementia (DLB) is a common form of cognitive impairment, accounting for 30% of dementia cases in ages over 65 years. Early diagnosis of DLB has been challenging; particularly in the context of differentiation with Parkinson’s disease dementia ...
Tayyabah Yousaf, G. Dervenoulas, Polytimi-Eleni Valkimadi, M. Politis   +3 more
semanticscholar   +1 more source

Early Retinal UCHL1 Dysregulation Coupled With Synaptic Loss Reflects Alzheimer's Disease Severity

Advanced Science, EarlyView.
This study identifies synapse‐enriched deubiquitinase UCHL1 as an early Aβ‐responsive regulator of retinal synaptopathy in Alzheimer's disease. Retinal UCHL1 loss accompanies excitatory synapse degeneration, p75NTR activation, and neuroinflammation, and predicts Braak stage and cognitive decline. Aβ42 fibrils trigger synaptic and UCHL1 depletion before
Altan Rentsendorj, Jean‐Philippe Vit, Alexandre Hutton, Yosef Koronyo, Saba Shahin, Edward Robinson, Ernesto Barron, Anthony Rodriguez, Ousman Jallow, Julia Sheyn, Bhakta Prasad Gaire, Lalita Subedi, Miyah R. Davis, Barathan Gnanabharathi, Alexander V. Ljubimov, Stuart L. Graham, Vivek K. Gupta, Mehdi Mirzaei, Debra Hawes, Katlin Silm, Keith L. Black, Lon S. Schneider, Alfredo A. Sadun, Jesse G. Meyer, Dieu‐Trang Fuchs, Maya Koronyo‐Hamaoui   +25 more
wiley   +1 more source

Environmental risk factors provoke new thinking for prevention and treatment of dementia with Lewy bodies

Heliyon
In recent years, environmental factors have received attention in the pathogenesis of neurodegenerative diseases. Other than genetic factors, the identification of environmental factors and modifiable risk factors may create opportunities to delay the ...
Dinghao An, Yun Xu
doaj   +1 more source

Phosphorylation of Ser-129 Is the Dominant Pathological Modification of α-Synuclein in Familial and Sporadic Lewy Body Disease*

Journal of Biological Chemistry, 2006
A comprehensive, unbiased inventory of synuclein forms present in Lewy bodies from patients with dementia with Lewy bodies was carried out using two-dimensional immunoblot analysis, novel sandwich enzyme-linked immunosorbent assays with modification ...
John P. Anderson, D. Walker, J. Goldstein, Rian de Laat, Kelly Banducci, R. Caccavello, R. Barbour, Ji-Ping Huang, Kristin Kling, Michael K. Lee, L. Diep, P. Keim, Xiaofeng Shen, T. Chataway, M. Schlossmacher, P. Seubert, D. Schenk, S. Sinha, W. Gai, T. Chilcote   +19 more
semanticscholar   +1 more source

TAB2 Causes Neuronal Damage by Aggravating Microglia‐Mediated Neuroinflammation in Parkinson's Disease

Advanced Science, EarlyView.
In microglia, STAT3 upregulates TAB2, which promotes NF‐κB activation through its NZF domain‐mediated recognition of K63‐linked ubiquitin chains, leading to inflammatory cytokine release and subsequent neuronal injury. Lumacaftor suppresses TAB2 expression and directly binds the TAB2‐NZF domain to interrupt K63 ubiquitin recognition, thereby blocking ...
Yanhao Zhao, Zimeng Huang, Jianing Gao, Aolan Li, Huizhi Wang, Yingchuan Chen, Guanyu Zhu, Xin Zhang, Yin Jiang, Moxuan Zhang, Fangang Meng, Jianguo Zhang, Tingting Du   +12 more
wiley   +1 more source

Association of cardiovascular disease management drugs with Lewy body dementia: a case–control study [PDF]

Lewy body dementia is the second most common neurodegenerative dementia after Alzheimer’s disease. Disease-modifying therapies for this disabling neuropsychiatric condition are critically needed.
Moroz, Brian E, The American Genome Center, Chia, Ruth, Cahoon, Elizabeth K, Pfeiffer, Ruth M, Dalgard, Clifton L, Freedman, Daryl Michal, International Lewy Body Dementia Genomics Consortium, Scholz, Sonja W, Saez-Atienzar, Sara   +9 more
core   +1 more source

Tau Aggregate Imaging and Transcriptomics of Alzheimer's Disease Brain at Different Stages of Disease

Advanced Science, EarlyView.
The protein aggregates and gene expression in the middle temporal gyrus (MTG) and somatosensory cortex (SOM) of the postmortem brains of 13 Alzheimer's disease patients were studied in detail, revealing that small hyperphosphorylated tau aggregates increase with Braak stage driven by microglial inflammation.
Elizabeth A. English, Dorothea Böken, Matthew W. Cotton, Matthew R. Cheetham, Johanna S. Jackson, Georg Meisl, John S. H. Danial, Paul M. Matthews, Nurun N. Fancy, David Klenerman   +9 more
wiley   +1 more source

Distinct patterns of amyloid‐dependent tau accumulation in Lewy body diseases

Movement Disorders, 2018
Background: In addition to Lewy body pathology, amyloid‐β plaques and neurofibrillary tangles that are characteristic for Alzheimer's disease are also frequently found in Lewy body diseases.
Seung-Ha Lee, Hanna Cho, J. Choi, J. H. Lee, Y. Ryu, M. Lee, C. Lyoo   +6 more
semanticscholar   +1 more source