Abstract
Understanding the pathophysiology and treatment of Alzheimer's disease is vitally important. Alzheimer's disease threatens to affect currently at least 30% of all individuals currently alive in the 12 most financially developed countries, unless interventions are discovered to prevent or treat the disease. Although memory loss is the cardinal symptom of Alzheimer's disease, the pathophysiological mechanisms leading to cognitive deficits are poorly understood. It is difficult to address this problem in human studies, and impossible in cultured cells. Therefore, animal models are needed to elucidate the molecular mechanisms leading to dementia. A large number of animal models have focussed upon the role of amyloid plaques in the pathogenesis of Alzheimer's disease, because amyloid plaques are an essential diagnostic feature of the disease. However, the mechanism by which amyloid plaques or their principal molecular constituent, the amyloid-ß protein (Aß), disrupt cognitive function is not well understood. Herein, I describemy perspective on what we have learned about howAß impairs memory from research on Alzheimer's disease in mice and rats.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 123-126 |
| Number of pages | 4 |
| Journal | Journal of Alzheimer's Disease |
| Volume | 9 |
| Issue number | SUPPL. 3 |
| State | Published - Jul 2006 |
Fingerprint
Keywords
- Aβ oligomers
- Memory
- Mice
- Morris water maze
- Operant behavioral task
- Rats
- Transgenic
Cite this
Molecular basis of memory loss in the TG2576 mouse model of Alzheimer's disease. / Ashe, Karen H.
In: Journal of Alzheimer's Disease, Vol. 9, No. SUPPL. 3, 07.2006, p. 123-126.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Molecular basis of memory loss in the TG2576 mouse model of Alzheimer's disease
AU - Ashe, Karen H.
PY - 2006/7
Y1 - 2006/7
N2 - Understanding the pathophysiology and treatment of Alzheimer's disease is vitally important. Alzheimer's disease threatens to affect currently at least 30% of all individuals currently alive in the 12 most financially developed countries, unless interventions are discovered to prevent or treat the disease. Although memory loss is the cardinal symptom of Alzheimer's disease, the pathophysiological mechanisms leading to cognitive deficits are poorly understood. It is difficult to address this problem in human studies, and impossible in cultured cells. Therefore, animal models are needed to elucidate the molecular mechanisms leading to dementia. A large number of animal models have focussed upon the role of amyloid plaques in the pathogenesis of Alzheimer's disease, because amyloid plaques are an essential diagnostic feature of the disease. However, the mechanism by which amyloid plaques or their principal molecular constituent, the amyloid-ß protein (Aß), disrupt cognitive function is not well understood. Herein, I describemy perspective on what we have learned about howAß impairs memory from research on Alzheimer's disease in mice and rats.
AB - Understanding the pathophysiology and treatment of Alzheimer's disease is vitally important. Alzheimer's disease threatens to affect currently at least 30% of all individuals currently alive in the 12 most financially developed countries, unless interventions are discovered to prevent or treat the disease. Although memory loss is the cardinal symptom of Alzheimer's disease, the pathophysiological mechanisms leading to cognitive deficits are poorly understood. It is difficult to address this problem in human studies, and impossible in cultured cells. Therefore, animal models are needed to elucidate the molecular mechanisms leading to dementia. A large number of animal models have focussed upon the role of amyloid plaques in the pathogenesis of Alzheimer's disease, because amyloid plaques are an essential diagnostic feature of the disease. However, the mechanism by which amyloid plaques or their principal molecular constituent, the amyloid-ß protein (Aß), disrupt cognitive function is not well understood. Herein, I describemy perspective on what we have learned about howAß impairs memory from research on Alzheimer's disease in mice and rats.
KW - Aβ oligomers
KW - Memory
KW - Mice
KW - Morris water maze
KW - Operant behavioral task
KW - Rats
KW - Transgenic
UR - http://www.scopus.com/inward/record.url?scp=33747431588&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=33747431588&partnerID=8YFLogxK
M3 - Article
C2 - 16914850
AN - SCOPUS:84880186891
VL - 9
SP - 123
EP - 126
JO - Journal of Alzheimer's Disease
JF - Journal of Alzheimer's Disease
SN - 1387-2877
IS - SUPPL. 3
ER -