Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 2 de 2
Filter
Add more filters











Database
Language
Publication year range
1.
Cell Mol Neurobiol ; 43(5): 1849-1865, 2023 Jul.
Article in English | MEDLINE | ID: mdl-36326951

ABSTRACT

Mitochondria are critical to multiple cellular processes, from the production of adenosine triphosphate (ATP), maintenance of calcium homeostasis, synthesis of key metabolites, and production of reactive oxygen species (ROS) to maintain necrosis, apoptosis, and autophagy. Therefore, proper clearance and regulation are essential to maintain various physiological processes carried out by the cellular mechanism, including mitophagy and autophagy, by breaking down the damaged intracellular connections under the influence of various genes and proteins and protecting against various neurodegenerative diseases such as Parkinson disease (PD), amyotrophic lateral sclerosis (ALS), Alzheimer disease (AD), and Huntington disease (HD). In this review, we will discuss the role of autophagy, selective macroautophagy, or mitophagy, and its role in neurodegenerative diseases along with normal physiology. In addition, this review will provide a better understanding of the pathways involved in neuron autophagy and mitophagy and how mutations affect these pathways in the various genes involved in neurodegenerative diseases. Various new findings indicate that the pathways that remove dysfunctional mitochondria are impaired in these diseases, leading to the deposition of damaged mitochondria. Apart from that, we have also discussed the therapeutic strategies targeting autophagy and mitophagy in neurodegenerative diseases. The mitophagy cycle results in the degradation of damaged mitochondria and the biogenesis of new healthy mitochondria, also highlighting different stages at which a particular neurodegenerative disease could occur.


Subject(s)
Neurodegenerative Diseases , Parkinson Disease , Humans , Mitophagy/physiology , Neurodegenerative Diseases/metabolism , Mitochondria/metabolism , Parkinson Disease/metabolism , Autophagy/physiology
2.
Curr Drug Targets ; 23(9): 913-923, 2022.
Article in English | MEDLINE | ID: mdl-35240956

ABSTRACT

Chemobrain is one of the major side effects of chemotherapy; despite increased research, the mechanisms underlying chemotherapy-induced cognitive changes remain unknown. Several possibly important candidate mechanisms have been identified and will be studied further in the future. Chemobrain is characterized by memory loss, cognitive impairment, difficulty in language, concentration, acceleration, and learning. The major characteristic of chemobrain is oxidative stress, mitochondrial dysfunction, immune dysregulation, hormonal alteration, white matter abnormalities, and DNA damage. Berberine (BBR) is an isoquinoline alkaloid extracted from various berberine species. BBR is a small chemical that easily passes the blood-brain barrier (BBB), making it useful for treating neurodegenerative diseases. Many studies on the pharmacology of BBR have been reported in the past. Furthermore, several clinical and experimental research indicates that BBR has a variety of pharmacological effects. So, in this review, we explore the pathogenesis of chemobrain and the neuroprotective potential of BBR against chemobrain. We also introduced the therapeutic role of BBR in various neurodegenerative and neurological diseases such as Alzheimer's, Parkinson's disease, mental depression, schizophrenia, anxiety, and also some stroke.


Subject(s)
Berberine , Chemotherapy-Related Cognitive Impairment , Cognitive Dysfunction , Neuroprotective Agents , Berberine/pharmacology , Berberine/therapeutic use , Cognitive Dysfunction/chemically induced , Cognitive Dysfunction/drug therapy , Humans , Neuroprotective Agents/adverse effects , Oxidative Stress
SELECTION OF CITATIONS
SEARCH DETAIL