TY - CHAP
T1 - Chapter 5.5 Transgenic mouse models of Alzheimer's disease and episodic-like memory
AU - Borchelt, David R.
AU - Savonenko, Alena V.
N1 - Copyright:
Copyright 2009 Elsevier B.V., All rights reserved.
PY - 2008
Y1 - 2008
N2 - In this chapter, we discuss examples of behavioral studies of several transgenic models of Alzheimer's-type amyloidosis, providing examples of approaches and comparisons of outcomes for reference, episodic-like, and working memory. Most studies have attempted to link changes in the levels of Aβ peptides (the primary component of senile plaques in Alzheimer's disease) to the onset of deficits in one type of memory, focusing on one behavioral task to assess specific cognitive functions. Studies that have analyzed concurrent changes in different memory systems have shown that tasks requiring flexible use of information "what," "where," and/or "when" (the episodic-like memory tasks) are useful in detecting losses in memory function. In general, impairments in episodic-like memory were detected earlier than in reference memory and were highly correlated with amyloid plaque load. An analysis of the literature, including our own studies, indicates that the accumulation of Aβ peptides impacts the cognitive functions of mice differentially as a function of age and Aβ amyloid load. Cognitive decline appears to be gradually progressive with parallels to human patients in that episodic-like memory is the first memory system affected. More importantly, the physical form of Aβ peptide (monomer, soluble oligomer, or fibril) that mediates memory deficits may differ at various stages of the disease, a finding that could alter strategies for treatment for this disease.
AB - In this chapter, we discuss examples of behavioral studies of several transgenic models of Alzheimer's-type amyloidosis, providing examples of approaches and comparisons of outcomes for reference, episodic-like, and working memory. Most studies have attempted to link changes in the levels of Aβ peptides (the primary component of senile plaques in Alzheimer's disease) to the onset of deficits in one type of memory, focusing on one behavioral task to assess specific cognitive functions. Studies that have analyzed concurrent changes in different memory systems have shown that tasks requiring flexible use of information "what," "where," and/or "when" (the episodic-like memory tasks) are useful in detecting losses in memory function. In general, impairments in episodic-like memory were detected earlier than in reference memory and were highly correlated with amyloid plaque load. An analysis of the literature, including our own studies, indicates that the accumulation of Aβ peptides impacts the cognitive functions of mice differentially as a function of age and Aβ amyloid load. Cognitive decline appears to be gradually progressive with parallels to human patients in that episodic-like memory is the first memory system affected. More importantly, the physical form of Aβ peptide (monomer, soluble oligomer, or fibril) that mediates memory deficits may differ at various stages of the disease, a finding that could alter strategies for treatment for this disease.
KW - Aβ amyloid plaques
KW - episodic-like memory
KW - progression of memory deficits
KW - reference memory
KW - working memory
UR - http://www.scopus.com/inward/record.url?scp=67649757582&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=67649757582&partnerID=8YFLogxK
U2 - 10.1016/S1569-7339(08)00230-0
DO - 10.1016/S1569-7339(08)00230-0
M3 - Chapter
AN - SCOPUS:67649757582
SN - 9780444531742
T3 - Handbook of Behavioral Neuroscience
SP - 553
EP - 573
BT - Handbook of Episodic Memory
A2 - Dere, Ekrem
A2 - Huston, Joseph
A2 - Easton, Alexander
A2 - Nadel, Lynn
ER -