Neuroprotective Role of Polyphenols in Treatment of Neurological Disorders: A Review

: The most frequent illnesses characterized by the gradual malfunctioning of brain neurons are neurodegenerative disorders (NDs). Genetic mutations and a range of biological processes can produce NDs. Alzheimer's disease (AD), Parkinson's disease (PD), and Multiple Sclerosis (MS) are all related to oxidative stress (OS). Reduced brain activity has become a greater health threat with a growing elderly population. It causes some pathophysiological alterations and is an important risk factor for a range of neurodegenerative illnesses. An increase in reactive oxygen species (ROS) can cause neuronal cell death, and it is thus essential to control ROS levels to maintain normal neuronal activity. Synthetic medicines are often used to treat neurological disorders; however, harmful effects have been reported. Multiple bodies of research have shown the effectiveness of polyphenols in the treatment of various NDs due to their negligible side effects. This review article describes the neuroprotection effects of polyphenols such as resveratrol, epigallocatechin-3-gallate, curcumin, and quercetin, as well as the signaling pathways and immune response controls through polyphenols.

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Mechanisms of Metal-Induced Mitochondrial Dysfunction in Neurological Disorders

Toxics ◽

10.3390/toxics9060142 ◽

2021 ◽

Vol 9 (6) ◽

pp. 142

Author(s):

Hong Cheng ◽

Bobo Yang ◽

Tao Ke ◽

Shaojun Li ◽

Xiaobo Yang ◽

...

Keyword(s):

Nervous System ◽

Mitochondrial Dysfunction ◽

Neurological Disorders ◽

Brain Function ◽

Energy Production ◽

Neuronal Cell Death ◽

Neuronal Cell ◽

Oxygen Species ◽

Subsequent Decrease ◽

The Brain

Metals are actively involved in multiple catalytic physiological activities. However, metal overload may result in neurotoxicity as it increases formation of reactive oxygen species (ROS) and elevates oxidative stress in the nervous system. Mitochondria are a key target of metal-induced toxicity, given their role in energy production. As the brain consumes a large amount of energy, mitochondrial dysfunction and the subsequent decrease in levels of ATP may significantly disrupt brain function, resulting in neuronal cell death and ensuing neurological disorders. Here, we address contemporary studies on metal-induced mitochondrial dysfunction and its impact on the nervous system.

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Death-Associated Protein Kinase 1 Phosphorylation in Neuronal Cell Death and Neurodegenerative Disease

International Journal of Molecular Sciences ◽

10.3390/ijms20133131 ◽

2019 ◽

Vol 20 (13) ◽

pp. 3131 ◽

Cited By ~ 11

Author(s):

Nami Kim ◽

Dongmei Chen ◽

Xiao Zhen Zhou ◽

Tae Ho Lee

Keyword(s):

Cell Death ◽

Protein Kinase ◽

Neurodegenerative Diseases ◽

Molecular Mechanisms ◽

Neuronal Cell Death ◽

Neuronal Cell ◽

Biological Processes ◽

Death Associated Protein Kinase ◽

The Brain

Regulated neuronal cell death plays an essential role in biological processes in normal physiology, including the development of the nervous system. However, the deregulation of neuronal apoptosis by various factors leads to neurodegenerative diseases such as ischemic stroke and Alzheimer’s disease (AD). Death-associated protein kinase 1 (DAPK1) is a calcium/calmodulin (Ca2+/CaM)-dependent serine/threonine (Ser/Thr) protein kinase that activates death signaling and regulates apoptotic neuronal cell death. Although DAPK1 is tightly regulated under physiological conditions, DAPK1 deregulation in the brain contributes to the development of neurological disorders. In this review, we describe the molecular mechanisms of DAPK1 regulation in neurons under various stresses. We also discuss the role of DAPK1 signaling in the phosphorylation-dependent and phosphorylation-independent regulation of its downstream targets in neuronal cell death. Moreover, we focus on the major impact of DAPK1 deregulation on the progression of neurodegenerative diseases and the development of drugs targeting DAPK1 for the treatment of diseases. Therefore, this review summarizes the DAPK1 phosphorylation signaling pathways in various neurodegenerative diseases.

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Chromosome Instability, Aging and Brain Diseases

Cells ◽

10.3390/cells10051256 ◽

2021 ◽

Vol 10 (5) ◽

pp. 1256

Author(s):

Ivan Y. Iourov ◽

Yuri B. Yurov ◽

Svetlana G. Vorsanova ◽

Sergei I. Kutsev

Keyword(s):

Brain Aging ◽

Chromosome Instability ◽

Neuronal Cell Death ◽

Neuronal Cell ◽

Accelerated Aging ◽

Brain Diseases ◽

Aging Brain ◽

Ontogenetic Changes ◽

Health And Disease

Chromosome instability (CIN) has been repeatedly associated with aging and progeroid phenotypes. Moreover, brain-specific CIN seems to be an important element of pathogenic cascades leading to neurodegeneration in late adulthood. Alternatively, CIN and aneuploidy (chromosomal loss/gain) syndromes exhibit accelerated aging phenotypes. Molecularly, cellular senescence, which seems to be mediated by CIN and aneuploidy, is likely to contribute to brain aging in health and disease. However, there is no consensus about the occurrence of CIN in the aging brain. As a result, the role of CIN/somatic aneuploidy in normal and pathological brain aging is a matter of debate. Still, taking into account the effects of CIN on cellular homeostasis, the possibility of involvement in brain aging is highly likely. More importantly, the CIN contribution to neuronal cell death may be responsible for neurodegeneration and the aging-related deterioration of the brain. The loss of CIN-affected neurons probably underlies the contradiction between reports addressing ontogenetic changes of karyotypes within the aged brain. In future studies, the combination of single-cell visualization and whole-genome techniques with systems biology methods would certainly define the intrinsic role of CIN in the aging of the normal and diseased brain.

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