scholarly journals Functional Impairment in Miro Degradation and Mitophagy Is a Shared Feature in Familial and Sporadic Parkinson’s Disease

2016 ◽  
Vol 19 (6) ◽  
pp. 709-724 ◽  
Author(s):  
Chung-Han Hsieh ◽  
Atossa Shaltouki ◽  
Ashley E. Gonzalez ◽  
Alexandre Bettencourt da Cruz ◽  
Lena F. Burbulla ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Functional Impairment ◽  
Shared Feature ◽  
Sporadic Parkinson’S Disease

Analysis of Functional and Cognitive Impairment in Institutionalized Individuals with Movement Disorders

2019 ◽  
Vol 19 (7) ◽  
pp. 1022-1031 ◽  
Author(s):  
Paula D. Cebrián ◽  
Omar Cauli
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Cognitive Impairment ◽  
Activities Of Daily Living ◽  
Cognitive Performance ◽  
Functional Impairment ◽  
Movement Disorders ◽  
Neurological Disorders ◽  
Daily Living ◽  
Severe Cognitive Impairment

Background: Many neurological disorders lead to institutionalization and can be accompanied in their advanced stages by functional impairment, and progressive loss of mobility, and cognitive alterations. Objective: We analyzed the relationship between functional impairment and cognitive performance and its related subdomains in individuals with Parkinson’s disease, Alzheimer’s disease accompanied by motor dysfunction, and with other neurological disorders characterized by both motor and cognitive problems. Methods: All participants lived in nursing homes (Valencia, Spain) and underwent cognitive evaluation with the Mini-Mental State Examination; functional assessment of independence in activities of daily living using the Barthel score and Katz index; and assessment of mobility with the elderly mobility scale. Results: The mean age of the subjects was 82.8 ± 0.6 years, 47% of the sample included individuals with Parkinson’s disease, and 48 % of the sample presented severe cognitive impairment. Direct significant relationships were found between the level of cognitive impairment and functional capacity (p < 0.01) and mobility (p < 0.05). Among the different domains, memory impairment was not associated with altered activities of daily living or mobility. The functional impairment and the risk of severe cognitive impairment were significantly (p<0.05) higher in female compared to male patients. Among comorbidities, overweight/obesity and diabetes were significantly (p < 0.05) associated with poor cognitive performance in those individuals with mild/moderate cognitive impairment. Conclusion: In institutionalized individuals with movement disorders there is an association between functional and cognitive impairment. Reduction of over-weight and proper control of diabetes may represent novel targets for improving cognitive function at such early stages.

scholarly journals The Nigral Coup in Parkinson’s Disease by α-Synuclein and Its Associated Rebels

Cells ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 598
Author(s):  
Jeswinder Sian-Hulsmann ◽  
Peter Riederer
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Viral Infections ◽  
Genetic Defect ◽  
Lewy Bodies ◽  
Common Denominator ◽  
Metabolic Disturbances ◽  
Trigger Factors ◽  
Protein Clearance ◽  
Sporadic Parkinson’S Disease

The risk of Parkinson’s disease increases with age. However, the etiology of the illness remains obscure. It appears highly likely that the neurodegenerative processes involve an array of elements that influence each other. In addition, genetic, endogenous, or exogenous toxins need to be considered as viable partners to the cellular degeneration. There is compelling evidence that indicate the key involvement of modified α-synuclein (Lewy bodies) at the very core of the pathogenesis of the disease. The accumulation of misfolded α-synuclein may be a consequence of some genetic defect or/and a failure of the protein clearance system. Importantly, α-synuclein pathology appears to be a common denominator for many cellular deleterious events such as oxidative stress, mitochondrial dysfunction, dopamine synaptic dysregulation, iron dyshomeostasis, and neuroinflammation. These factors probably employ a common apoptotic/or autophagic route in the final stages to execute cell death. The misfolded α-synuclein inclusions skillfully trigger or navigate these processes and thus amplify the dopamine neuron fatalities. Although the process of neuroinflammation may represent a secondary event, nevertheless, it executes a fundamental role in neurodegeneration. Some viral infections produce parkinsonism and exhibit similar characteristic neuropathological changes such as a modest brain dopamine deficit and α-synuclein pathology. Thus, viral infections may heighten the risk of developing PD. Alternatively, α-synuclein pathology may induce a dysfunctional immune system. Thus, sporadic Parkinson’s disease is caused by multifactorial trigger factors and metabolic disturbances, which need to be considered for the development of potential drugs in the disorder.

scholarly journals Parkin interacting substrate zinc finger protein 746 is a pathological mediator in Parkinson’s disease

Brain ◽  
2019 ◽  
Vol 142 (8) ◽  
pp. 2380-2401 ◽  
Author(s):  
Saurav Brahmachari ◽  
Saebom Lee ◽  
Sangjune Kim ◽  
Changqing Yuan ◽  
Senthilkumar S Karuppagounder ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Critical Role ◽  
Trna Synthetase ◽  
Loss Of Function ◽  
Substrate Protein ◽  
Finger Protein ◽  
Sporadic Parkinson’S Disease

Abstract α-Synuclein misfolding and aggregation plays a major role in the pathogenesis of Parkinson’s disease. Although loss of function mutations in the ubiquitin ligase, parkin, cause autosomal recessive Parkinson’s disease, there is evidence that parkin is inactivated in sporadic Parkinson’s disease. Whether parkin inactivation is a driver of neurodegeneration in sporadic Parkinson’s disease or a mere spectator is unknown. Here we show that parkin in inactivated through c-Abelson kinase phosphorylation of parkin in three α-synuclein-induced models of neurodegeneration. This results in the accumulation of parkin interacting substrate protein (zinc finger protein 746) and aminoacyl tRNA synthetase complex interacting multifunctional protein 2 with increased parkin interacting substrate protein levels playing a critical role in α-synuclein-induced neurodegeneration, since knockout of parkin interacting substrate protein attenuates the degenerative process. Thus, accumulation of parkin interacting substrate protein links parkin inactivation and α-synuclein in a common pathogenic neurodegenerative pathway relevant to both sporadic and familial forms Parkinson’s disease. Thus, suppression of parkin interacting substrate protein could be a potential therapeutic strategy to halt the progression of Parkinson’s disease and related α-synucleinopathies.

Contribution of coding/non-coding variants in NUS1 to late-onset sporadic Parkinson's disease

2021 ◽  
Vol 84 ◽  
pp. 29-34
Author(s):  
Li Jiang ◽  
Hong-xu Pan ◽  
Yu-wen Zhao ◽  
Qian Zeng ◽  
Zhen-hua Liu ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Late Onset ◽  
Sporadic Parkinson’S Disease ◽  
Coding Variants

A novel and functional variant within the ATG5 gene promoter in sporadic Parkinson's disease

2013 ◽  
Vol 538 ◽  
pp. 49-53 ◽  
Author(s):  
Dongfeng Chen ◽  
Cuiping Zhu ◽  
Xuenan Wang ◽  
Xungang Feng ◽  
Shuchao Pang ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Gene Promoter ◽  
Functional Variant ◽  
Sporadic Parkinson’S Disease

Association of ZNF184, IL1R2, LRRK2, ITPKB, and PARK16 with sporadic Parkinson’s disease in Eastern China

2020 ◽  
Vol 735 ◽  
pp. 135261
Author(s):  
Ting Gao ◽  
Ran Zheng ◽  
Yang Ruan ◽  
Yi Fang ◽  
Chongyao Jin ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Eastern China ◽  
Sporadic Parkinson’S Disease
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