Animals share the challenge of maintaining an internal environment
that is restricted to fairly low ranges of temperature, pH, and
water content within a well-protected envelope while engaged in
continuous exchanges with the environment in terms of gases,
liquids, energy, even as movement of body parts and the entire
organism itself is necessary for survival. This dynamic spectrum of
changes is further amplified during developmental events or more
acutely during responses to pernicious environmental factors in due
to trauma and disease. In addition, persistent incidents associated
with aging can result in irreversible changes to the allostasis
that characterizes the living condition.
In the nervous system, a very high metabolic turnover, fragile
but steep ionic gradients, and morphological and structural
constraints dictated by the necessity for prompt neuronal
transmission of electrical impulses and necessary plasticity result
in a highly fragile organ system.
Here we address a small sampling of major constituents of neural
function at the cellular and molecular level that play important
roles in development and aging, two endogenous processes that
embody features of allostasis or the dynamic shifts in set points
for specific homeostatic mechanisms associated with development and
aging.
The opening chapters discuss the major players in the
neurotrophic hypothesis, the neurotrophins. These growth factors
have been shown to play a significant role during development and
in the maintenance of the adult cholinergic system in CNS as well
as in the development of the sensory and sympathetic nervous
system. That they are also involved in plasticity events associated
with memoryand behavior points to the degenerate nature of
signaling molecules that archive specificity by acting in concert
as part of ensembles of molecules rather than solitary
regulators.
It is widely known that oligodendroglia and myelination events
are late arrivals in the developmental scheme of the brain and are
also prime targets in early development of ischemic insults. Thus,
a chapter on oligodendroglia and myelination in development and
aging serves to introduce these nonneuronal partners vital to
proper neuronal transmission. Molecular participants in stress
responses to both acute and chronic stressors are discussed from
different perspectives in following chapters with varying degrees
of emphasis on injury versus normal aging and neurodegenerative
disease.
The study of neural responses to stress of various kinds has led
to a realization of the importance of plasticity and the complexity
of the mechanism allowing plasticity in the nervous system. The
chapters addressing the topic are followed by an introduction to
the amyloid hypothesis, and what may be its central character the
enzyme held mostly responsible for the generation of beta amyloid.
This if followed by a broader discussion of misfolding proteins in
the nervous system and its possible interventions to counteract
aging-associated deficits.
Limited in scope but offering a broad sampling, these chapters
stress the dynamic features of neuronal responses to internal
(developmental) cues or the more harmful external events (injury
and disease) in a modern perspective.
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