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 - Modulation of β-amyloid production and fibrillisation
AU - Allsop, David
AU - Twyman, Lance
AU - Davies, Yvonne
AU - Moore, Susan
AU - York, Amber
AU - Swanson, Linda
AU - Soutar, Ian
PY - 2000
Y1 - 2000
N2 - Alzheimer’s disease (AD) is the most common cause of dementia in old age and presently affects an estimated 4 million people in the U.S.A. and 0.75 million people in the U.K. It is a relentless, degenerative brain disease, characterized by progressive cognitive impairment. In the final stages of the disease, patients are often bedridden, doubly incontinent and unable to speak or to recognize close relatives. Pathological changes of Alzheimer’s disease include extensive neuronal loss and the presence of numerous neurofibrillary tangles and senile plaques in the brain. The senile plaques contain amyloid fibrils derived from a 39-43-amino-acid peptide referred to as b-amyloid or Ab. The basic theory of the so-called ‘amyloid hypothesis’ is that the deposition of aggregated forms of Ab in the brain parenchyma triggers a pathological cascade of events that leads to neurofibrillary tangle formation, neuronal loss and the associated dementia [1]. Here we discuss progress towards the identification of inhibitors of Ab production and fibrillization.
AB - Alzheimer’s disease (AD) is the most common cause of dementia in old age and presently affects an estimated 4 million people in the U.S.A. and 0.75 million people in the U.K. It is a relentless, degenerative brain disease, characterized by progressive cognitive impairment. In the final stages of the disease, patients are often bedridden, doubly incontinent and unable to speak or to recognize close relatives. Pathological changes of Alzheimer’s disease include extensive neuronal loss and the presence of numerous neurofibrillary tangles and senile plaques in the brain. The senile plaques contain amyloid fibrils derived from a 39-43-amino-acid peptide referred to as b-amyloid or Ab. The basic theory of the so-called ‘amyloid hypothesis’ is that the deposition of aggregated forms of Ab in the brain parenchyma triggers a pathological cascade of events that leads to neurofibrillary tangle formation, neuronal loss and the associated dementia [1]. Here we discuss progress towards the identification of inhibitors of Ab production and fibrillization.
M3 - Literature review
VL - 67
SP - 1
EP - 14
JO - Biochemical Society Symposia
JF - Biochemical Society Symposia
SN - 1744-1439
ER -