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Small molecule inhibitors of Aβ-aggregation and neurotoxicity

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Small molecule inhibitors of Aβ-aggregation and neurotoxicity. / Hawkes, Cheryl A.; Ng, Vivian; McLaurin, Joanne.
In: Drug Development Research, Vol. 70, No. 2, 01.03.2009, p. 111-124.

Research output: Contribution to Journal/MagazineJournal articlepeer-review

Harvard

Hawkes, CA, Ng, V & McLaurin, J 2009, 'Small molecule inhibitors of Aβ-aggregation and neurotoxicity', Drug Development Research, vol. 70, no. 2, pp. 111-124. https://doi.org/10.1002/ddr.20290

APA

Hawkes, C. A., Ng, V., & McLaurin, J. (2009). Small molecule inhibitors of Aβ-aggregation and neurotoxicity. Drug Development Research, 70(2), 111-124. https://doi.org/10.1002/ddr.20290

Vancouver

Hawkes CA, Ng V, McLaurin J. Small molecule inhibitors of Aβ-aggregation and neurotoxicity. Drug Development Research. 2009 Mar 1;70(2):111-124. Epub 2009 Feb 27. doi: 10.1002/ddr.20290

Author

Hawkes, Cheryl A. ; Ng, Vivian ; McLaurin, Joanne. / Small molecule inhibitors of Aβ-aggregation and neurotoxicity. In: Drug Development Research. 2009 ; Vol. 70, No. 2. pp. 111-124.

Bibtex

@article{34b9ceef716b4a2baaf9197f389751c3,
title = "Small molecule inhibitors of Aβ-aggregation and neurotoxicity",
abstract = "Alzheimer disease (AD) is characterized pathologically by extracellular amyloid deposits composed of Aβ peptide, neurofibrillary tangles (NFTs) made up of hyperphosphorylated tau, and a deficit of cholinergic neurons in the basal forebrain. Presently, only symptomatic therapies are available for the treatment of AD and these therapies have a limited time frame of utility. Amyloid disorders represent the effects of chronic Aβ production and are not a secondary pathological effect caused by a distant trigger; therefore targeting Aβ is a viable pursuit. In this review, we will discuss the various small molecule anti- aggregation inhibitors that have been reported in the literature, with emphasis on compounds that are presently being investigated in clinical trials.",
keywords = "Aggregation, Alzheimer's disease, Amyloid, Inhibitors",
author = "Hawkes, {Cheryl A.} and Vivian Ng and Joanne McLaurin",
year = "2009",
month = mar,
day = "1",
doi = "10.1002/ddr.20290",
language = "English",
volume = "70",
pages = "111--124",
journal = "Drug Development Research",
issn = "0272-4391",
publisher = "John Wiley and Sons Inc.",
number = "2",

}

RIS

TY - JOUR

T1 - Small molecule inhibitors of Aβ-aggregation and neurotoxicity

AU - Hawkes, Cheryl A.

AU - Ng, Vivian

AU - McLaurin, Joanne

PY - 2009/3/1

Y1 - 2009/3/1

N2 - Alzheimer disease (AD) is characterized pathologically by extracellular amyloid deposits composed of Aβ peptide, neurofibrillary tangles (NFTs) made up of hyperphosphorylated tau, and a deficit of cholinergic neurons in the basal forebrain. Presently, only symptomatic therapies are available for the treatment of AD and these therapies have a limited time frame of utility. Amyloid disorders represent the effects of chronic Aβ production and are not a secondary pathological effect caused by a distant trigger; therefore targeting Aβ is a viable pursuit. In this review, we will discuss the various small molecule anti- aggregation inhibitors that have been reported in the literature, with emphasis on compounds that are presently being investigated in clinical trials.

AB - Alzheimer disease (AD) is characterized pathologically by extracellular amyloid deposits composed of Aβ peptide, neurofibrillary tangles (NFTs) made up of hyperphosphorylated tau, and a deficit of cholinergic neurons in the basal forebrain. Presently, only symptomatic therapies are available for the treatment of AD and these therapies have a limited time frame of utility. Amyloid disorders represent the effects of chronic Aβ production and are not a secondary pathological effect caused by a distant trigger; therefore targeting Aβ is a viable pursuit. In this review, we will discuss the various small molecule anti- aggregation inhibitors that have been reported in the literature, with emphasis on compounds that are presently being investigated in clinical trials.

KW - Aggregation

KW - Alzheimer's disease

KW - Amyloid

KW - Inhibitors

U2 - 10.1002/ddr.20290

DO - 10.1002/ddr.20290

M3 - Journal article

AN - SCOPUS:64349107868

VL - 70

SP - 111

EP - 124

JO - Drug Development Research

JF - Drug Development Research

SN - 0272-4391

IS - 2

ER -