Clinical neuropsychological assessment in older adults with Lewy body disease and Parkinson's disease.

2018 ◽  
pp. 277-299
Author(s):  
Julie A. Fields
Keyword(s):  
Older Adults ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Neuropsychological Assessment ◽  
Lewy Body ◽  
Lewy Body Disease

scholarly journals Inflammation in mild cognitive impairment due to Parkinson's disease, Lewy body disease, and Alzheimer's disease

2019 ◽  
Vol 34 (8) ◽  
pp. 1244-1250 ◽  
Author(s):  
Eleanor King ◽  
John O'Brien ◽  
Paul Donaghy ◽  
Caroline H. Williams-Gray ◽  
Rachael A. Lawson ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Parkinson’S Disease ◽  
Alzheimer's Disease ◽  
Parkinson's Disease ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Lewy Body ◽  
Lewy Body Disease

scholarly journals Olfactory dysfunction in incidental Lewy body disease and Parkinson's disease

2014 ◽  
Vol 20 (11) ◽  
pp. 1260-1262 ◽  
Author(s):  
Erika Driver-Dunckley ◽  
Charles H. Adler ◽  
Joseph G. Hentz ◽  
Brittany N. Dugger ◽  
Holly A. Shill ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Lewy Body ◽  
Lewy Body Disease ◽  
Olfactory Dysfunction ◽  
Incidental Lewy Body Disease

scholarly journals It Is Time to Study Overlapping Molecular and Circuit Pathophysiologies in Alzheimer’s and Lewy Body Disease Spectra

2021 ◽  
Vol 15 ◽  
Author(s):  
Noritaka Wakasugi ◽  
Takashi Hanakawa
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Continuous Spectrum ◽  
Lewy Body ◽  
Lewy Bodies ◽  
Amyloid Β ◽  
Lewy Body Disease ◽  
Common Mechanism ◽  
Protein Accumulation ◽  
The Brain

Alzheimer’s disease (AD) is the leading cause of dementia due to neurodegeneration and is characterized by extracellular senile plaques composed of amyloid β1–42 (Aβ) as well as intracellular neurofibrillary tangles consisting of phosphorylated tau (p-tau). Dementia with Lewy bodies constitutes a continuous spectrum with Parkinson’s disease, collectively termed Lewy body disease (LBD). LBD is characterized by intracellular Lewy bodies containing α-synuclein (α-syn). The core clinical features of AD and LBD spectra are distinct, but the two spectra share common cognitive and behavioral symptoms. The accumulation of pathological proteins, which acquire pathogenicity through conformational changes, has long been investigated on a protein-by-protein basis. However, recent evidence suggests that interactions among these molecules may be critical to pathogenesis. For example, Aβ/tau promotes α-syn pathology, and α-syn modulates p-tau pathology. Furthermore, clinical evidence suggests that these interactions may explain the overlapping pathology between AD and LBD in molecular imaging and post-mortem studies. Additionally, a recent hypothesis points to a common mechanism of prion-like progression of these pathological proteins, via neural circuits, in both AD and LBD. This suggests a need for understanding connectomics and their alterations in AD and LBD from both pathological and functional perspectives. In AD, reduced connectivity in the default mode network is considered a hallmark of the disease. In LBD, previous studies have emphasized abnormalities in the basal ganglia and sensorimotor networks; however, these account for movement disorders only. Knowledge about network abnormalities common to AD and LBD is scarce because few previous neuroimaging studies investigated AD and LBD as a comprehensive cohort. In this paper, we review research on the distribution and interactions of pathological proteins in the brain in AD and LBD, after briefly summarizing their clinical and neuropsychological manifestations. We also describe the brain functional and connectivity changes following abnormal protein accumulation in AD and LBD. Finally, we argue for the necessity of neuroimaging studies that examine AD and LBD cases as a continuous spectrum especially from the proteinopathy and neurocircuitopathy viewpoints. The findings from such a unified AD and Parkinson’s disease (PD) cohort study should provide a new comprehensive perspective and key data for guiding disease modification therapies targeting the pathological proteins in AD and LBD.

110 Atrophy of the mediodorsal thalamus is associated with visual hallucinations in lewy body diseases

2018 ◽  
Vol 89 (6) ◽  
pp. A43.3-A44
Author(s):  
Elie Matar ◽  
Daniel Brooks ◽  
Antony Harding ◽  
Glenda Halliday
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Lewy Body ◽  
Neuronal Degeneration ◽  
Neuronal Loss ◽  
Lewy Body Disease ◽  
Visual Hallucinations ◽  
Volume Loss ◽  
Thalamic Nuclei ◽  
Mediodorsal Thalamus

IntroductionAlthough limbic system dysfunction has been thought to underlie visual hallucinations in patients with Lewy body disorders, neuropathology within thalamic structures subserving limbic functions have not been examined. In this study, we assessed the degree of neuronal degeneration in thalamic regions involved in perceptual integration in patients with Parkinson’s disease (PD), Parkinson’s disease dementia (PDD) and dementia with Lewy bodies (DLB).MethodsPost-mortem samples were acquired from twenty-four individuals with Lewy body disease (5 PD, 9 PDD, 10 DLB) and 10 age-matched controls. The anterior principal (AP) and mediodorsal (MD) thalamic nuclei were delineated and analysed using stereological and quantitative neuropathological techniques.ResultsVolume loss within the MD nucleus was observed in patients with DLB (31%) and PDD (18%) but not PD compared to controls (ANOVA, p<0.05). The atrophy was significantly greater in those patients with hallucinations than those without (p<0.05). Somal atrophy was seen in all patient groups and did not correlate with volume loss or visual hallucinations. Interestingly, there was no neuronal loss in this region compared to controls in the Lewy body disease groups. Analysis of the AP nucleus revealed similar patterns of volume loss but with somal atrophy only in patients with PDD and DLB. Both these measures did not correlate significantly with visual hallucinations, but was significantly different in patients with dementia compared to PD only and controls (p<0.05).ConclusionThese results suggest that afferent denervation of the mediodorsal thalamus may contribute to visual hallucinations. This appears to support models that implicate upstream components of the limbic circuitry in the generation of this phenomenon.

scholarly journals Evidence for angiogenesis in Parkinson’s disease, incidental Lewy body disease, and progressive supranuclear palsy

2011 ◽  
Vol 119 (1) ◽  
pp. 59-71 ◽  
Author(s):  
Brinda Desai Bradaric ◽  
Aditiben Patel ◽  
Julie A. Schneider ◽  
Paul M. Carvey ◽  
Bill Hendey
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Progressive Supranuclear Palsy ◽  
Lewy Body ◽  
Lewy Body Disease ◽  
Incidental Lewy Body Disease
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