经化学和分子神经生物学手册 第3版 Handbook of Neurochemistry and Molecular Neurobiology
This volume deals with nervous system injuries, repair and therapeutic approaches, and some neurodegenerative
diseases not covered in other volumes of the Handbook. How current research changed our
understanding of the epidemiology, pathophysiological mechanisms, cell demise leading to loss of function,
whether in traumatic brain injury (TBI), spinal cord injury (SCI), or neurodegenerative diseases, and
therapeutic approaches to ameliorate dysfunction of these devastating conditions are emphasized. Central
nervous system (CNS) trauma (TBI and SCI combined) is one of the major causes of death in the United
States and is one of the main killers (perhaps number one) of the young people below the mid-thirties.While
TBI kills the majority of these victims, SCI, depending on the severity, leads to lifelong disability and despair
at the time of their highest productivity. One of the most important areas in medicine now is the repair of the
damaged tissue of injured brain and spinal cord so the function may be improved or restored. The major
problem facing clinicians and researchers is the failure of brain and spinal cord to repair or regenerate the
damaged areas, perhaps because these organs are so overly complex, functionally and structurally, containing
different cell types, fiber pathways, messengers (neurochemicals), and other elements. In addition, damage
to tissue in trauma is caused by not one, but many multi-destructive pathways.
In spite of this complexity, neuroscience has made significant advances in understanding of the delayed
injury process (i.e. secondary damage), providing opportunities for target-based therapeutic intervention,
improved imaging, blood vessel growth, regeneration, and tissue transplantation, including stem cell
application. During the last two decades of vigorous research, scientists have identified several secondary
injury factors, although many still remain unknown, that damage or destroy injured brain and spinal cord.
They are trying to understand how these factors, including increased calcium and calcium-mediated events
(namely lipases and proteases), free radicals, excitotoxicity, alterations in structural integrity of cell
membrane, axonal damage in white matter, and reduction in blood flow, lead to apoptosis and necrosis
of neurons and myelinating oligodendrocytes and ultimately destruction of tissue following injury.
Although better imaging and pharmacological therapy using methylprednisolone and surgical manipulation,
particularly in SCI, have slightly improved the clinical management of patients, we are still nowhere
near acknowledging any real recovery of function. Yes, advances have been made over the years. Yet, we
know little and much needs to be learned about how to reduce disability and restore function in TBI and
SCI. Therefore, vigorous research is needed in other areas, including regeneration, protection of cells
and preservation of axons, imaging by distension tensor imaging (DTI) and restoring blood supply that
may help further improve function following TBI and SCI. Some of these detrimental pathways may be
common to neurodegenerative disease such as Alzheimer’s disease (AD), Parkinson’s disease (PD), multiple
sclerosis (MS), and amyotrophic lateral sclerosis (ALS), which will also benefit from this research attenuating
dysfunction.
请点击此处下载
收藏
