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Emerging beta-amyloid therapies for the treatment of Alzheimer's disease.
Curr Pharm Des. 2003; 9(6):427-47.CP

Abstract

Alzheimer's Disease (AD) is a progressive neurodegenerative disorder marked by loss of memory, cognition, and behavioral stability. AD is defined pathologically by extracellular neuritic plaques comprised of fibrillar deposits of beta-amyloid peptide (Abeta) and neurofibrillary tangles comprised of paired helical filaments of hyperphosphorylated tau. Current therapies for AD, such as cholinesterase inhibitors, treat the symptoms but do not modify the progression of the disease. The etiology of AD is unclear. However, data from familial AD mutations (FAD) strongly support the "amyloid cascade hypothesis" of AD, i.e. that neurodegeneration in AD is initiated by the formation of neurotoxic beta-amyloid (Abeta) aggregates; all FAD mutations increase levels of Abeta peptide or density of Abeta deposits. The likely link between Abeta aggregation and AD pathology emphasizes the need for a better understanding of the mechanisms of Abeta production. This review summarizes current therapeutic strategies directed at lowering Abeta levels and decreasing levels of toxic Abeta aggregates through (1) inhibition of the processing of amyloid precursor protein (APP) to Abeta peptide, (2) inhibition, reversal or clearance of Abeta aggregation, (3) cholesterol reduction and (4) Abeta immunization.

Authors+Show Affiliations

Conway KA
Drug Discovery Division, Johnson & Johnson Pharmaceutical Research and Development, Spring House, PA 19477, USA. kconway3@prdus.jnj.com
Baxter EW
No affiliation info available
Felsenstein KM
No affiliation info available
Reitz AB
No affiliation info available

MeSH

Alzheimer DiseaseAmyloid Precursor Protein SecretasesAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAnimalsAnti-Bacterial AgentsApolipoproteins EAspartic Acid EndopeptidasesCholesterolDrug DesignEndopeptidasesHumansImmunotherapy, ActiveMiceMice, TransgenicPolymorphism, Genetic

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

12570807

Citation

Conway, Kelly A., et al. "Emerging Beta-amyloid Therapies for the Treatment of Alzheimer's Disease." Current Pharmaceutical Design, vol. 9, no. 6, 2003, pp. 427-47.
Conway KA, Baxter EW, Felsenstein KM, et al. Emerging beta-amyloid therapies for the treatment of Alzheimer's disease. Curr Pharm Des. 2003;9(6):427-47.
Conway, K. A., Baxter, E. W., Felsenstein, K. M., & Reitz, A. B. (2003). Emerging beta-amyloid therapies for the treatment of Alzheimer's disease. Current Pharmaceutical Design, 9(6), 427-47.
Conway KA, et al. Emerging Beta-amyloid Therapies for the Treatment of Alzheimer's Disease. Curr Pharm Des. 2003;9(6):427-47. PubMed PMID: 12570807.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Emerging beta-amyloid therapies for the treatment of Alzheimer's disease. AU - Conway,Kelly A, AU - Baxter,Ellen W, AU - Felsenstein,Kevin M, AU - Reitz,Allen B, PY - 2003/2/7/pubmed PY - 2003/6/14/medline PY - 2003/2/7/entrez SP - 427 EP - 47 JF - Current pharmaceutical design JO - Curr Pharm Des VL - 9 IS - 6 N2 - Alzheimer's Disease (AD) is a progressive neurodegenerative disorder marked by loss of memory, cognition, and behavioral stability. AD is defined pathologically by extracellular neuritic plaques comprised of fibrillar deposits of beta-amyloid peptide (Abeta) and neurofibrillary tangles comprised of paired helical filaments of hyperphosphorylated tau. Current therapies for AD, such as cholinesterase inhibitors, treat the symptoms but do not modify the progression of the disease. The etiology of AD is unclear. However, data from familial AD mutations (FAD) strongly support the "amyloid cascade hypothesis" of AD, i.e. that neurodegeneration in AD is initiated by the formation of neurotoxic beta-amyloid (Abeta) aggregates; all FAD mutations increase levels of Abeta peptide or density of Abeta deposits. The likely link between Abeta aggregation and AD pathology emphasizes the need for a better understanding of the mechanisms of Abeta production. This review summarizes current therapeutic strategies directed at lowering Abeta levels and decreasing levels of toxic Abeta aggregates through (1) inhibition of the processing of amyloid precursor protein (APP) to Abeta peptide, (2) inhibition, reversal or clearance of Abeta aggregation, (3) cholesterol reduction and (4) Abeta immunization. SN - 1381-6128 UR - https://www.unboundmedicine.com/medline/citation/12570807/Emerging_beta_amyloid_therapies_for_the_treatment_of_Alzheimer's_disease_ DB - PRIME DP - Unbound Medicine ER -