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.
Highlights
Aging is a physiological, progressive, and time-dependent process that results in accumulated changes at the cellular and molecular levels
The present study reports detailed ultrastructural examinations of hippocampal synapses in young and old rats
Morphometric analysis of the Transmission Electron Microscopy (TEM) images further revealed that energy production by the synaptic mitochondria, as determined by calculating the coefficient of energy efficiency of mitochondria (CEEM) of the CA1 region of the hippocampus, reduced by 42.4% (Figure 5) in old compared to Antioxidants 2019, 8, x FOR PEER R EVIEW
Summary
Progressive, and time-dependent process that results in accumulated changes at the cellular and molecular levels. The brain is highly sensitive to the aging process, as many neurodegenerative diseases clearly show [1,2,3]. The hippocampus is especially vulnerable to damage at the early stage of aging [4], which results in the development of several age-dependent neurodegenerative disorders, including Parkinson’s and Alzheimer’s diseases [5,6]. While the age-related decline in hippocampal volume has been well documented, most knowledge of hippocampal relationships between structure and function has been discovered in the context of neurological and neurodegenerative diseases [11,12]. The relationship between cognitive aging and hippocampal structure in the absence of disease remains relatively understudied
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