Research output: Contribution to Journal/Magazine › Literature review › peer-review
Research output: Contribution to Journal/Magazine › Literature review › peer-review
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TY - JOUR
T1 - Amyloid β-peptide and Alzheimer's disease
AU - Allsop, David
AU - Mayes, Jennifer
PY - 2014/8/18
Y1 - 2014/8/18
N2 - One of the hallmarks of Alzheimer’s disease (AD) is the formation of senile plaques in the brain, which contain fibrils composed of the amyloid-β (Aβ) peptide. According to the ‘amyloid cascade’ hypothesis, the aggregation of Aβ initiates a sequence of events leading to the formation of neurofibrillary tangles, neurodegeneration, and on to the main symptom of dementia. However, emphasis has now shifted away from fibrillar forms of Aβ and towards smaller and more soluble ‘oligomers’ as the main culprit in AD. The present chapter commences with a brief introduction to the disease and its current treatment, and then focuses on the formation Aβ from the amyloid precursor protein (APP), the genetics of early-onset AD, which has provided strong support for the amyloid cascade hypothesis, and then on the development of new drugs aimed at reducing the load of cerebral Aβ, which are still the main hope for providing a more effective treatment for AD in the future.
AB - One of the hallmarks of Alzheimer’s disease (AD) is the formation of senile plaques in the brain, which contain fibrils composed of the amyloid-β (Aβ) peptide. According to the ‘amyloid cascade’ hypothesis, the aggregation of Aβ initiates a sequence of events leading to the formation of neurofibrillary tangles, neurodegeneration, and on to the main symptom of dementia. However, emphasis has now shifted away from fibrillar forms of Aβ and towards smaller and more soluble ‘oligomers’ as the main culprit in AD. The present chapter commences with a brief introduction to the disease and its current treatment, and then focuses on the formation Aβ from the amyloid precursor protein (APP), the genetics of early-onset AD, which has provided strong support for the amyloid cascade hypothesis, and then on the development of new drugs aimed at reducing the load of cerebral Aβ, which are still the main hope for providing a more effective treatment for AD in the future.
KW - amyloid cascade
KW - genetics
KW - oligomer
KW - secretase
KW - senile plaque
KW - treatment
U2 - 10.1042/bse0560099
DO - 10.1042/bse0560099
M3 - Literature review
VL - 56
SP - 99
EP - 110
JO - Essays in Biochemistry
JF - Essays in Biochemistry
SN - 0071-1365
M1 - 7
ER -