Visit our Expo - Redox and Inflammation signaling 2012

Session XII : Cell death and neurodegenerative diseases Poster XII, 4
Preservation of mitochondrial volume homeostasis at the early stages of age-related
synaptic deterioration
Carlo Bertoni-Freddari, Patrizia Fattoretti, Belinda Giorgetti, Yessica Grossi, Marta
Balietti, Tiziana Casoli, Giuseppina Di Stefano, *Gemma Perretta
Neurobiology of Aging Laboratory, INRCA Research Department, Via Birarelli 8,
60121 Ancona, Italy Email: c.bertoni@inrca.it and *Istituto di Neurobiologia e
Medicina Molecolare-CNR, S.p Anguillarese km 1.3, 00060 Roma, Italy
A morphometric study on synaptic mitochondria was performed in the frontal (FC) and
temporal (TC) cortex of adult (mean age: 10.6 years) and aged (mean age: 20.8 years)
monkeys (Macaca fascicularis). In order to identify ultrastructural alterations due to age, the
average mitochondrial size (average volume: V), the overall volume covered by mitochondria
(volume density: Vv) and the number of mitochondria per cubic micron of tissue (numeric
density: Nv) were measured. Either in FC and TC no significant age-related differences were
revealed for any of the above mentioned morphometric parameters. Namely, in FC of aged
monkeys a decrease of Nv (6%) and Vv (2%) was observed, whereas V showed an increase
by 5%. In TC of aged animals, both Nv and Vv increased by 7% and V was decreased by 2%.
While the observed changes in FC are in general agreement with data previously reported on
age-related changes in mitochondrial ultrastructure with reference to TC an opposite trend
was shown. Mitochondria are very plastic organelles capable of consistent rearrangements of
their morphology in reaction to different environmental stimuli. Accordingly, V, Nv and Vv
account for changes in single aspects of mitochondrial ultrastructure, nonetheless, when
considered together per experimental group, they might represent an index of the structural
rearrangements occurring on discrete pools of organelles (in this study, those located at the
synaptic terminals). On the basis of these assumptions, the present findings document a
preservation of the mitocondrial volume homeostasis in the brain of aged monkeys. Since our
data from a previous investigation on the same animals showed early signs of synaptic
deterioration in FC and TC during aging, this seems to be in contrast with the results obtained
in the present study. However, an age-related preservation of the mitochondrial potential for
structural dynamics may be interpreted as a reactive response to an altered synaptic function.
We suggest that mitochondria might represent sensitive targets for therapeutic interventions
aimed at counteracting early events of synaptic critical alterations able to trigger the
pathogenesis of neurodegenerative diseases.
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