Biomedical Engineering Reference
In-Depth Information
Fig. 1. Known and suggested interactions between mitochondrial dynamics, ROS, misfolded proteins, and low levels of
mtDNA deletions with neurodegenerative processes.
Solid black arrows
indicate known interactions whereas
dashed
arrows
indicate suggested ones.
Controversy and interest lies in which types of disruptions are
causal or possibly secondary to this eventual undesirable cell death
(Fig.
1
).
This introductory chapter will highlight key findings on four
different types of mitochondrial malfunctions and their relation
to neurodegenerative disease. Defects in mitochondrial dynamics,
mutations in the mitochondrial genome, the creation and pres-
ence of reactive oxygen species, and protein aggregate-associated
dysfunctions of mitochondria exemplify how different stressors to
this important organelle can contribute to neurodegenerative
disease.
2. Mitochondrial
Dynamics and
Importance to
Neuronal Function
and Physiology
Mitochondria are not static organelles suspended in isolation
inside of the cell; they are dynamic. There are two aspects related
to mitochondrial dynamics in neurons. (1) Mitochondrial move-
ment along axons and dendritic processes. (2) Mitochondrial
fusion and fission. Both the compartmentalization inside of the
neuron and dynamics of mitochondrial fission and fusion are
extremely important to their neuronal functioning.
As a highly polarized cell, the neuron has different physiolog-
ical properties and demands for bioenergetic needs regionalized
in certain locations. Anterograde mitochondrial transport to
mobilize mitochondria into presynaptic terminals is necessary for
normal neuronal function, health, and electrophysiological prop-
erties needed to reverse ion fluxes and alter Ca
+2
signaling
demanded by synaptic transmission (
1
). Also, the presence of the
mitochondria at this locale allows it to provide ATP that is used
to mobilize the vesicle reserve pool during high frequency
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