Linking Heat Shock Protein 70 and Parkin in Parkinson’s Disease

Zhao, Zhenjun; Zheng, Lan; Du, Fangning; Wang, Yixin; Wu, Yue; Lim, Kah‐Leong; Lin, Lin; Yang, Naidi; Zhang, Chengwu

doi:10.1007/s12035-023-03481-x

Cited by 3 publications

(2 citation statements)

References 150 publications

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“…This phenomenon is reversed by the use of a cFIR ceramic in our investigation [47]. FIR also induces heat shock proteins (HSPs) [48] that participate in the degradation of misfolded and aggregated proteins, identified as a pivotal role in the pathogenesis of PD [49]. HSPs prevent protein misfolding while inhibiting the apoptosis involved in PD pathogenesis [50].…”

Section: Discussionmentioning

confidence: 85%

Amelioration of Motor Performance and Nigrostriatal Dopamine Cell Volume Using a Novel Far-Infrared Ceramic Blanket in an A53T Alpha-Synuclein Transgenic Parkinson’s Disease Mouse Model

Carrick,

Hernandez,

Sugaya

2023

CIMB

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We had attended a Parkinson’s Disease (PD) patient for a non-healing wound who reported a marked decrease in his hand tremor and freezing of gait when his wound was exposed to a ceramic far-field infrared (cFIR) blanket. PD is the most frequent motor disorder and the second most frequent neurodegenerative disease after Alzheimer’s Disease (AD). The tremor, rigidity, and slowness of movement associated with Parkinson’s disease (PD) affect up to 10 million people throughout the world, and the major contributing factor to the pathogenesis of PD is the accumulation and propagation of pathological α-synuclein (α-Syn) and the death of dopaminergic cells in the Nigrostriatal system. Efforts to slow or stop its spreading have resulted in the development and use of dopaminergic drug replacement therapy. Unfortunately, there is a loss of about 70–80% of substantia nigral dopaminergic neurons in patients by the time they are diagnosed with PD, and various dopaminergic drugs provide only temporary relief of their motor symptoms. There are limitations in treating PD with many conventional medications, necessitating a combination of pharmaceutical and non-pharmacological therapy as an essential adjunct to better address the health and welfare of PD patients. We used male adult A53T alpha-synuclein transgenic mice exposed to a ceramic far-infrared blanket. Motor activity was assessed using the rotarod apparatus, and mouse brains were examined to quantify the fluorescence intensities of the immunostained samples. A53T alpha-synuclein transgenic mice had a significantly shorter time stay on the rotating bar than the wild-type mice (B6C3H). The rotarod performance was significantly improved in A53T alpha-synuclein transgenic mice exposed to cFIR as well as B6C3H healthy wild mice exposed to cFIR. There was a significant statistical and substantive increase in the cellular composition of the Striatum and substantia nigra of cFIR-treated mice. Improvement in motor performance is seen in PD mice and wild mice and is associated with increases in cell volume in the substantia nigra and striatum after treatment.

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Section: Discussionmentioning

confidence: 85%

Amelioration of Motor Performance and Nigrostriatal Dopamine Cell Volume Using a Novel Far-Infrared Ceramic Blanket in an A53T Alpha-Synuclein Transgenic Parkinson’s Disease Mouse Model

Carrick,

Hernandez,

Sugaya

2023

CIMB

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“…Numerous preclinical and clinical studies provide evidence that various molecular chaperones belonging to heat shock protein (HSP) families are either downregulated or dysfunctional in PD [106]. Molecular chaperones not only modulate α-syn but are also implicated in other PD-relevant proteins such as LRRK2 [107], PINK1 [108], PARKIN [109], and DJ-1 [110]. Notably, an increasing body of evidence supports the idea that HSPs directly interact with immune cells [111].…”

Section: Gut Microbiota Infections and Mitochondrial Dysfunction In Pdmentioning

confidence: 99%

The Role of Immune Dysfunction in Parkinson’s Disease Development

Cossu,

Hatano,

Hattori

2023

IJMS

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Recent research has unveiled intriguing insights suggesting that the body’s immune system may be implicated in Parkinson’s disease (PD) development. Studies have observed disparities in pro-inflammatory and anti-inflammatory markers between PD patients and healthy individuals. This finding underscores the potential influence of immune system dysfunction in the genesis of this condition. A dysfunctional immune system can serve as a primary catalyst for systemic inflammation in the body, which may contribute to the emergence of various brain disorders. The identification of several genes associated with PD, as well as their connection to neuroinflammation, raises the likelihood of disease susceptibility. Moreover, advancing age and mitochondrial dysfunction can weaken the immune system, potentially implicating them in the onset of the disease, particularly among older individuals. Compromised integrity of the blood–brain barrier could facilitate the immune system’s access to brain tissue. This exposure may lead to encounters with native antigens or infections, potentially triggering an autoimmune response. Furthermore, there is mounting evidence supporting the notion that gut dysbiosis might represent an initial trigger for brain inflammation, ultimately promoting neurodegeneration. In this comprehensive review, we will delve into the numerous hypotheses surrounding the role of both innate and adaptive immunity in PD.

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The Role of Immune Dysfunction in Parkinson's Disease Development

Cossu,

Hatano,

Hattori

2023

Preprint

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Recent research has unveiled intriguing insights suggesting that the body's immune system may be implicated in Parkinson's disease (PD) development. Studies have observed disparities in pro-inflammatory and anti-inflammatory markers between PD patients and healthy individuals. This finding underscores the potential influence of immune system dysfunction in the genesis of this condition. A dysfunctional immune system can serve as a primary catalyst for systemic in-flammation in the body, which may contribute to the emergence of various brain disorders. The identification of several genes associated with PD, as well as their connection to neuroinflamma-tion, raises the likelihood of disease susceptibility. Moreover, advancing age and mitochondrial dysfunction can weaken the immune system, potentially implicating them in the onset of the dis-ease, particularly among older individuals. Compromised integrity of the blood-brain barrier could facilitate the immune system's access to brain tissue. This exposure may lead to encounters with native antigens or infections, potentially triggering an autoimmune response. Furthermore, there is mounting evidence supporting the notion that gut dysbiosis might represent an initial trigger for brain inflammation, ultimately promoting neurodegeneration. In this comprehensive review, we will delve into the numerous hypotheses surrounding the role of both innate and adaptive immunity in PD.

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Linking Heat Shock Protein 70 and Parkin in Parkinson’s Disease

Cited by 3 publications

References 150 publications

Amelioration of Motor Performance and Nigrostriatal Dopamine Cell Volume Using a Novel Far-Infrared Ceramic Blanket in an A53T Alpha-Synuclein Transgenic Parkinson’s Disease Mouse Model

Amelioration of Motor Performance and Nigrostriatal Dopamine Cell Volume Using a Novel Far-Infrared Ceramic Blanket in an A53T Alpha-Synuclein Transgenic Parkinson’s Disease Mouse Model

The Role of Immune Dysfunction in Parkinson’s Disease Development

The Role of Immune Dysfunction in Parkinson's Disease Development

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