Alzheimer disease: 100 years later
Almost 100 years since the first clinical report of a case of Alzheimer disease (AD), three early-onset and two late-onset AD genes have been identified. While rare mutations in the early-onset genes (amyloid precursor protein, and presenilins 1 and 2) lead to increased generation of specific forms...
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Sociedad Médica de Santiago
2001
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oai:scielo:S0034-988720010005000152005-11-24Alzheimer disease: 100 years laterPuglielli MD,LuigiM Kovacs PhD,Dora Alzheimer disease Amyloid beta-Protein Genetics, biochemical Molecular biology Almost 100 years since the first clinical report of a case of Alzheimer disease (AD), three early-onset and two late-onset AD genes have been identified. While rare mutations in the early-onset genes (amyloid precursor protein, and presenilins 1 and 2) lead to increased generation of specific forms of the amyloid ß protein (A,ß), common polymorphisms in the late-onset genes (apolipoprotein E and alpha²-macroglobulin) are thought to alter the clearance and degradation of A,ß in brain. Although definite proof for a direct link between altered A ß generation/clearance and neurodegeneration has not yet been attained, mechanism-based approaches for the therapeutic treatment of AD based on lowering levels of the potentially pathogenic Aß are currently underway. The recent discovery of the enzymes (secretases) responsible for generating Aß have paved the way for the development of such drugs and increase the prospects for successful therapeutic intervention to arrest AD neuropathogenesis (Rev Méd Chile 2001; 129: 569-75)info:eu-repo/semantics/openAccessSociedad Médica de SantiagoRevista médica de Chile v.129 n.5 20012001-05-01text/htmlhttp://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0034-98872001000500015en10.4067/S0034-98872001000500015 |
institution |
Scielo Chile |
collection |
Scielo Chile |
language |
English |
topic |
Alzheimer disease Amyloid beta-Protein Genetics, biochemical Molecular biology |
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Alzheimer disease Amyloid beta-Protein Genetics, biochemical Molecular biology Puglielli MD,Luigi M Kovacs PhD,Dora Alzheimer disease: 100 years later |
description |
Almost 100 years since the first clinical report of a case of Alzheimer disease (AD), three early-onset and two late-onset AD genes have been identified. While rare mutations in the early-onset genes (amyloid precursor protein, and presenilins 1 and 2) lead to increased generation of specific forms of the amyloid ß protein (A,ß), common polymorphisms in the late-onset genes (apolipoprotein E and alpha²-macroglobulin) are thought to alter the clearance and degradation of A,ß in brain. Although definite proof for a direct link between altered A ß generation/clearance and neurodegeneration has not yet been attained, mechanism-based approaches for the therapeutic treatment of AD based on lowering levels of the potentially pathogenic Aß are currently underway. The recent discovery of the enzymes (secretases) responsible for generating Aß have paved the way for the development of such drugs and increase the prospects for successful therapeutic intervention to arrest AD neuropathogenesis (Rev Méd Chile 2001; 129: 569-75) |
author |
Puglielli MD,Luigi M Kovacs PhD,Dora |
author_facet |
Puglielli MD,Luigi M Kovacs PhD,Dora |
author_sort |
Puglielli MD,Luigi |
title |
Alzheimer disease: 100 years later |
title_short |
Alzheimer disease: 100 years later |
title_full |
Alzheimer disease: 100 years later |
title_fullStr |
Alzheimer disease: 100 years later |
title_full_unstemmed |
Alzheimer disease: 100 years later |
title_sort |
alzheimer disease: 100 years later |
publisher |
Sociedad Médica de Santiago |
publishDate |
2001 |
url |
http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0034-98872001000500015 |
work_keys_str_mv |
AT pugliellimdluigi alzheimerdisease100yearslater AT mkovacsphddora alzheimerdisease100yearslater |
_version_ |
1718435973167054848 |