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2009 | 69 | 3 |
Tytuł artykułu

Therapeutic approaches targeting betta-amyloid cascade in Alzheimer's disease

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Warianty tytułu
Języki publikacji
EN
Abstrakty
EN
Alzheimer’s disease (AD) is the most common cause of dementia, affecting nearly fi ve million patients in the USA and 20 million worldwide. The β-amyloid (Aβ) cascade hypothesis maintains that accumulation of Aβ peptide is a critical event in the early pathogenesis of AD. This lecture will review key steps of Aβ metabolism and their disturbances leading to build-up of Aβ in the AD brain. Development of therapeutic approaches targeting Aβ cascade will be subsequently discussed. They include passive and active immunization against Aβ, inhibitors of β and γ secretases, RAGE inhibitors, β-sheet breakers and approaches targeting the apolipoprotein E (apoE). ApoE is a critical factor promoting Aβ deposition in the brain and affecting its clearance. The magnitude of the apoE/Aβ interaction is isoform specifi c, providing an explanation for the linkage between the apoE4 allele and an increased risk of sporadic AD. Our laboratory has demonstrated that blocking the apoE/Aβ binding with synthetic peptide-Aβ12-28P, which mimics the apoE binding site on Aβ, reduces the burden of vascular and parenchymal Aβ deposits in AD transgenic mice and prevents them from developing a memory defi cit. Ongoing research pursues development of peptidomimetic derivatives of Aβ12-28P with improved therapeutic effi cacy and biostability with the aim to obtain a lead therapeutic compound for clinical investigations. Support: Dorothy D. Eweson Lectureship on the Advances in Aging Research, grants AG24847, AG31221
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-
Rocznik
Tom
69
Numer
3
Opis fizyczny
p.286
Twórcy
autor
  • Department of Neurology, Pharmacology and Psychiatry, New York University School of Medicine, New York, NY, USA
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Typ dokumentu
Bibliografia
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