Mechanisms underlying neuronal dysfunction and degeneration caused by loss of presynaptic mitochondria

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K06712
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Neurophysiology / General neuroscience
• Research Institution: Tokyo Metropolitan University
• Principal Investigator: Ando Kanae (安藤香奈絵) 首都大学東京, 理工学研究科, 准教授 (40632500)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: ミトコンドリア / 神経細胞死 / 加齢 / 軸索輸送 / エネルギー代謝 / 神経変性疾患

Outline of Final Research Achievements

Brain nerve cells extend long processes to communicate with other cells. The contact sites are called synapses and demand energy supply to function. To meet the energy demands, mitochondria, tiny powerhouses in the cell, are transported from the cell body of the nerve cells. Depletion of mitochondria from the cells disrupts neuronal functions and eventually causes neuronal death. However, how the loss of synaptic mitochondria leads to neuronal death is not known. To elucidate the underlying molecular mechanisms, we used transgenic fruit fly to deplete mitochondria from synapses. We identified several molecules that are involved in neuronal dysfunction and cell loss triggered by loss of synaptic mitochondria. Since the loss of synaptic mitochondria is associated with neurodegenerative diseases such as Alzheimer’s disease, these findings may lead to development of a cure.

Free Research Field

神経科学、分子生物学、細胞生物学