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Modulation of β-amyloid production and fibrillisation

Research output: Contribution to journalLiterature review

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Modulation of β-amyloid production and fibrillisation. / Allsop, David; Twyman, Lance; Davies, Yvonne; Moore, Susan; York, Amber; Swanson, Linda; Soutar, Ian.

In: Biochemical Society Symposia, Vol. 67, 2000, p. 1-14.

Research output: Contribution to journalLiterature review

Harvard

Allsop, D, Twyman, L, Davies, Y, Moore, S, York, A, Swanson, L & Soutar, I 2000, 'Modulation of β-amyloid production and fibrillisation', Biochemical Society Symposia, vol. 67, pp. 1-14.

APA

Allsop, D., Twyman, L., Davies, Y., Moore, S., York, A., Swanson, L., & Soutar, I. (2000). Modulation of β-amyloid production and fibrillisation. Biochemical Society Symposia, 67, 1-14.

Vancouver

Allsop D, Twyman L, Davies Y, Moore S, York A, Swanson L et al. Modulation of β-amyloid production and fibrillisation. Biochemical Society Symposia. 2000;67:1-14.

Author

Allsop, David ; Twyman, Lance ; Davies, Yvonne ; Moore, Susan ; York, Amber ; Swanson, Linda ; Soutar, Ian. / Modulation of β-amyloid production and fibrillisation. In: Biochemical Society Symposia. 2000 ; Vol. 67. pp. 1-14.

Bibtex

@article{6dd40d54c275449da029bb09a18d60e1,
title = "Modulation of β-amyloid production and fibrillisation",
abstract = "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.",
author = "David Allsop and Lance Twyman and Yvonne Davies and Susan Moore and Amber York and Linda Swanson and Ian Soutar",
year = "2000",
language = "English",
volume = "67",
pages = "1--14",
journal = "Biochemical Society Symposia",
issn = "0067-8694",
publisher = "Portland Press Ltd.",

}

RIS

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 - 0067-8694

ER -