| Down syndrome and beta-amyloid deposition. | |
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MedLine Citation:
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PMID: 15021233 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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PURPOSE OF REVIEW: Exciting new therapeutic approaches to the treatment or prevention of Alzheimer's disease involve preventing, slowing or reversing beta-amyloid accumulation. These interventions may also apply to the treatment of Alzheimer's disease in Down syndrome. The purpose of the current review is therefore to summarize developments and advances in our understanding of beta-amyloid pathogenesis in Down syndrome over the past year. RECENT FINDINGS: A shift in research to a focus on early events in beta-amyloid pathogenesis in Down syndrome has led to several novel observations. Several authors have reported the accumulation of both soluble and intracellular beta-amyloid before extracellular beta-amyloid (senile plaques) in Down syndrome. Increases in beta-amyloid levels in Down syndrome may reflect the increased expression and protein levels of beta-site amyloid precursor protein cleavage enzyme 2 on chromosome 21. The impact of the accumulation of beta-amyloid may have differential effects on development and aging in Down syndrome. SUMMARY: The past year has seen significant advances in our understanding of beta-amyloid pathogenesis and the functional consequences of beta-amyloid accumulation in Down syndrome. However, there are still large gaps in our knowledge of the pathways involved in beta-amyloid degradation and clearance. It will be critical to conduct clinical trials to test therapeutic strategies that may reduce beta-amyloid in Down syndrome directly to determine the optimal age and dose for specific interventions. Given the differences in the mechanism of beta-amyloid accumulation in Down syndrome, careful consideration needs to be given to potential clinical trials to treat this disorder. |
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Authors:
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Elizabeth Head; Ira T Lott |
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Publication Detail:
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Type: Journal Article; Review |
Journal Detail:
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Title: Current opinion in neurology Volume: 17 ISSN: 1350-7540 ISO Abbreviation: Curr. Opin. Neurol. Publication Date: 2004 Apr |
Date Detail:
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Created Date: 2004-03-15 Completed Date: 2004-08-26 Revised Date: 2009-11-19 |
Medline Journal Info:
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Nlm Unique ID: 9319162 Medline TA: Curr Opin Neurol Country: England |
Other Details:
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Languages: eng Pagination: 95-100 Citation Subset: IM |
Affiliation:
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Institute for Brain Aging and Dementia, Department of Neurology, University of California, Irvine, California, USA. ehead@uci.edu |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Adult Alzheimer Disease / diagnosis, genetics, pathology Amyloid Precursor Protein Secretases Amyloid beta-Protein / metabolism* Amyloid beta-Protein Precursor / metabolism Amyloidosis, Familial / diagnosis, genetics*, pathology Aspartic Acid Endopeptidases / genetics* Brain / pathology Child Chromosomes, Human, Pair 21* Down Syndrome / diagnosis, genetics*, pathology Gene Expression Regulation, Enzymologic / physiology Humans Lipid Peroxidation / genetics, physiology Reactive Oxygen Species / metabolism Superoxide Dismutase / genetics, physiology |
| Chemical | |
Reg. No./Substance:
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0/Amyloid beta-Protein; 0/Amyloid beta-Protein Precursor; 0/Reactive Oxygen Species; EC 1.15.1.1/Superoxide Dismutase; EC 3.4.-/Amyloid Precursor Protein Secretases; EC 3.4.23.-/Aspartic Acid Endopeptidases |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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