TY - JOUR
T1 - Chapter 25 Neuronal responses to injury and aging
T2 - Lessons from animal models
AU - Price, Donald L.
AU - Koo, Edward H.
AU - Sisodia, Sangram S.
AU - Martin, Lee J.
AU - Koliatsos, Vassilis E.
AU - Muma, Nancy A.
AU - Walker, Lary C.
AU - Cork, Linda C.
N1 - Funding Information:
This work was supported by grants from the U.S. Public Health Service (NIH AG 03359, AG 05146, NS 17079, NS 20471) and funds from The Robert L. and Clara G. Patterson Trust and the American Health Assistance Foundation. Dr. Price is the recipient of a Javits Neuroscience Investigator Award (NIH NS 10580). Drs. Price, Muma, and Koo are recipients of a Leadership and Excellence in Alzheimer’s Disease (LEAD) award (NIA AG 07914).
PY - 1990/1/1
Y1 - 1990/1/1
N2 - 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 withinbrain 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.
AB - 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 withinbrain 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.
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U2 - 10.1016/S0079-6123(08)63186-6
DO - 10.1016/S0079-6123(08)63186-6
M3 - Article
C2 - 2087560
AN - SCOPUS:0025600394
SN - 0079-6123
VL - 86
SP - 297
EP - 308
JO - Progress in brain research
JF - Progress in brain research
IS - C
ER -