Skip to content
2000
Volume 4, Issue 2
  • ISSN: 1570-159X
  • E-ISSN: 1875-6190

Abstract

Brain atrophy caused by neuronal loss is a prominent pathological feature of Alzheimer's disease (AD). Amyloid (A ), the major component of senile plaques, is considered to play a central role in neuronal cell death. In addition to removal of the toxic Aβ , direct suppression of neuronal loss is an essential part of AD treatment; however, no such neuroprotective therapies have been developed. Excess amount of Aβ evokes multiple cytotoxic mechanisms, involving increase of the intracellular Ca2+ level, oxidative stress, and receptor-mediated activation of cell-death cascades. Such diversity in cytotoxic mechanisms induced by Aβ clearly indicates a complex nature of the AD-related neuronal cell death. We have identified a 24-residue peptide, Humanin (HN), which suppresses in vitro neuronal cell death caused by all AD-related insults, including Aβ , so far tested. The anti-AD effect of HN has been further confirmed in vivo using mice with Aβ -induced amnesia. Altogether, such potent neuroprotective activity of HN against AD-relevant cytotoxicity both in vitro and in vivo suggests the potential clinical applications of HN in novel AD therapies aimed at controlling neuronal death.

Loading

Article metrics loading...

/content/journals/cn/10.2174/157015906776359577
2006-04-01
2025-07-15
Loading full text...

Full text loading...

/content/journals/cn/10.2174/157015906776359577
Loading
This is a required field
Please enter a valid email address
Approval was a Success
Invalid data
An Error Occurred
Approval was partially successful, following selected items could not be processed due to error
Please enter a valid_number test