The Hsp70 Chaperone System in Parkinson’s Disease

Labrador-Garrido, Adahir; Bertoncini, Carlos W.; Roodveldt, Cintia

doi:10.5772/16671

Cited by 3 publications

(1 citation statement)

References 205 publications

(209 reference statements)

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“…61 Based on several reports, numerous results conducted on PD mechanism have indicated that HSP70 may solubilize α-syn and induce the degradation of its insoluble forms via chaperone-mediated autophagy and the proteasome. 62, 63…”

Section: Hsp70 In Neurodegeneration Diseasesmentioning

confidence: 99%

Impact of Heat Shock Proteins in Neurodegeneration: Possible Therapeutical Targets

Beretta

Shala

2022

Annals of Neurosciences

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Human neurodegenerative diseases occur as a result of various factors. Regardless of the variety in the etiology of development, many of these diseases are characterized by the accumulation of pathological, misfolded proteins; hence, such diseases are considered as proteinopathies. While plenty of research study has been conducted in order to identify the pathophysiology of these proteinopathies, there is still a lack of understanding in terms of potential therapeutic targets. Molecular chaperones present the main workforce for cellular protection and stress response. Therefore, considering these functions, molecular chaperones present a promising target for research within the field of conformational diseases that arise from proteinopathies. Since the association between neurodegenerative disorders and their long-term consequences is well documented, the need for the development of new therapeutic strategies becomes even more critical. In this review, we summarized the molecular function of heat shock proteins and recent progress on their role, involvement, and other mechanisms related to neurodegeneration caused by different etiological factors. Based on the relevant scientific data, we will highlight the functional classification of heat shock proteins, regulatin, and their therapeutic potential for neurodegenerative disorders.

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Section: Hsp70 In Neurodegeneration Diseasesmentioning

confidence: 99%

Impact of Heat Shock Proteins in Neurodegeneration: Possible Therapeutical Targets

Beretta

Shala

2022

Annals of Neurosciences

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Pla2g6 Deficiency in Zebrafish Leads to Dopaminergic Cell Death, Axonal Degeneration, Increased β-Synuclein Expression, and Defects in Brain Functions and Pathways

2018

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This study aimed to gain insights into the pathophysiology underlying PLA2G6-associated neurodegeneration that is implicated in three different neurological disorders, suggesting that other, unknown genetic or environmental factors might contribute to its wide phenotypic expression. To accomplish this, we downregulated the function of pla2g6 in the zebrafish nervous system, performed parkinsonism-related phenotypic characterization, and determined the effects of gene regulation upon the loss of pla2g6 function by using RNA sequencing and downstream analyses. Pla2g6 deficiency resulted in axonal degeneration, dopaminergic and motor neuron cell loss, and increased β-synuclein expression. We also observed that many of the identified, differentially expressed genes were implicated in other brain disorders, which might explain the variable phenotypic expression of pla2g6-associated disease, and found that top enriched canonical pathways included those already known or suggested to play a major role in the pathogenesis of Parkinson's disease. Our data support that pla2g6 is relevant for cranial motor development with significant implications in the pathophysiology underlying Parkinson's disease.

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Investigational surgical therapies

Issar¹

2013

Handbook of Parkinson’s Disease

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The Hsp70 Chaperone System in Parkinson’s Disease

Cited by 3 publications

References 205 publications

Impact of Heat Shock Proteins in Neurodegeneration: Possible Therapeutical Targets

Impact of Heat Shock Proteins in Neurodegeneration: Possible Therapeutical Targets

Pla2g6 Deficiency in Zebrafish Leads to Dopaminergic Cell Death, Axonal Degeneration, Increased β-Synuclein Expression, and Defects in Brain Functions and Pathways

Investigational surgical therapies

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