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The Role of Impaired Mitochondrial Transport in the Development of Neurodegenerative Diseases.
Blagov, Alexander; Borisov, Evgeny; Grechko, Andrey; Popov, Mikhail; Sukhorukov, Vasily; Orekhov, Alexander.
Afiliação
  • Blagov A; Laboratory of Angiopathology, Institute of General Pathology and Pathophysiology, 125315 Moscow, Russia.
  • Borisov E; Petrovsky Scientific Center of Surgery, 119991 Moscow, Russia.
  • Grechko A; Federal Research and Clinical Center of Intensive Care Medicine and Rehabilitology, 109240 Moscow, Russia.
  • Popov M; Department of Cardiac Surgery, Moscow Regional Research and Clinical Institute (MONIKI), 129110 Moscow, Russia.
  • Sukhorukov V; Petrovsky Scientific Center of Surgery, 119991 Moscow, Russia.
  • Orekhov A; Petrovsky Scientific Center of Surgery, 119991 Moscow, Russia.
J Integr Neurosci ; 22(4): 86, 2023 Jul 03.
Article em En | MEDLINE | ID: mdl-37519177
ABSTRACT
The fight against neurodegenerative diseases is one of the key direction of modern medicine. Unfortunately, the difficulties in understanding the factors underlying the development of neurodegeneration hinder the development of breakthrough therapeutics that can stop or at least greatly slow down the progression of these diseases. In this review, it is considered the disruption of mitochondrial transport as one of the pathogenesis factors contributing to neurodegeneration using the examples of Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, and Huntington's disease. Here, the mechanism of mitochondrial transport under normal conditions and the mechanisms of disturbances for the indicated diseases will be considered.
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Texto completo: 1 Base de dados: MEDLINE Assunto principal: Doença de Parkinson / Doença de Huntington / Doenças Neurodegenerativas / Doença de Alzheimer Limite: Humans Idioma: En Ano de publicação: 2023 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Doença de Parkinson / Doença de Huntington / Doenças Neurodegenerativas / Doença de Alzheimer Limite: Humans Idioma: En Ano de publicação: 2023 Tipo de documento: Article