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Antioxidants (Basel). 2019 Jun 11;8(6). pii: E171. doi: 10.3390/antiox8060171.

Transmission Electron Microscopy Study of Mitochondria in Aging Brain Synapses.

Author information

1
Department of Pharmacology and Physiology, Georgetown University Medical Center, Washington, DC 20057, USA. Vor5@georgetown.edu.
2
Department of Pharmacology and Physiology, Georgetown University Medical Center, Washington, DC 20057, USA. ys82@georgetown.edu.
3
Department of Pathological Anatomy N2, Bogomolets National Medical University, Kiev 01601, Ukraine. alexander.gavrysh@gmail.com.
4
Department of Pathological Anatomy N2, Bogomolets National Medical University, Kiev 01601, Ukraine. dibrova03@ukr.net.
5
Department of Pathological Anatomy N2, Bogomolets National Medical University, Kiev 01601, Ukraine. gychka59@gmail.com.
6
Department of Pharmacology and Physiology, Georgetown University Medical Center, Washington, DC 20057, USA. ns1015@georgetown.edu.

Abstract

The brain is sensitive to aging-related morphological changes, where many neurodegenerative diseases manifest accompanied by a reduction in memory. The hippocampus is especially vulnerable to damage at an early stage of aging. The present transmission electron microscopy study examined the synapses and synaptic mitochondria of the CA1 region of the hippocampal layer in young-adult and old rats by means of a computer-assisted image analysis technique. Comparing young-adult (10 months of age) and old (22 months) male Fischer (CDF) rats, the total numerical density of synapses was significantly lower in aged rats than in the young adults. This age-related synaptic loss involved degenerative changes in the synaptic architectonic organization, including damage to mitochondria in both pre- and post-synaptic compartments. The number of asymmetric synapses with concave curvature decreased with age, while the number of asymmetric synapses with flat and convex curvatures increased. Old rats had a greater number of damaged mitochondria in their synapses, and most of this was type II and type III mitochondrial structural damage. These results demonstrate age-dependent changes in the morphology of synaptic mitochondria that may underlie declines in age-related synaptic function and may couple to age-dependent loss of synapses.

KEYWORDS:

aging; brain; electron microscopy; hippocampus; mitochondria; synapse

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