Neuronal responses to injury and aging: lessons from animal models.
Alzheimer's disease (AD), the most common type of adult-onset dementia, is characterized by a variety of brain abnormalities, including degeneration of certain populations of nerve cells, alterations in the neuronal cytoskeleton, and the abnormal deposition of amyloid within brain parenchyma. Pathogenetic processes that lead to these brain abnormalities are difficult to study in humans. Recently, investigators have begun to utilize animal models to examine some of the mechanisms that cause cellular/molecular alterations in transmitter systems, cytoskeletal elements, and APP. These investigations have helped to clarify issues related to the lesions that occur in aged humans and individuals with AD.
Price
D L
DL
Neuropathology Laboratory, Johns Hopkins University School of Medicine, Baltimore, MD.
Koo
E H
EH
Sisodia
S S
SS
Martin
L J
LJ
Koliatsos
V E
VE
Muma
N A
NA
Walker
L C
LC
Cork
L C
LC
D000375:Aging / Q000502:physiology*; D000544:Alzheimer Disease / Q000503:physiopathology*; D016229:Amyloid beta-Peptides / Q000096:biosynthesis; D000818:Animals; D001369:Axons / Q000502:physiology*; D001522:Behavior, Animal; D002490:Central Nervous System / Q000293:injuries; D003599:Cytoskeleton / Q000378:metabolism / Q000648:ultrastructure; D004195:Disease Models, Animal; D006801:Humans; D008253:Macaca mulatta / Q000502:physiology; D009410:Nerve Degeneration; D009454:Neurofibrils / Q000648:ultrastructure; D009474:Neurons / Q000502:physiology*; D059348:Peripheral Nerve Injuries
D016229:Amyloid beta-Peptides