Year: 2014
Type: dissertation
Abstract: Alzheimer’s disease (AD), a progressive neurodegenerative disorder that affects mostly the \nlimbic system and the neocortical areas of the brain, is the most prevalent form of dementia \naffecting the elderly population. Twenty-nine million people live with the disease worldwide, \n10% of the population > 65 years of age and 50 % of the population > 85 years of age. These \nfigures are expected to increase exponentially over the next few decades and reach 81.1 million \nby the year 2040. Hallmark lesions include extracellular deposition of β-amyloid protein (Aβ) \nfibrillar plaques and intraneuronal neurofibrillary tangles (NFTs), which impair synaptic \nplasticity in the target regions of the brain thereby producing a progressive decline in cognitive \nfunction, with the earliest signs observed in learning and memory. Current therapies of AD are \nmerely palliative and only slow down cognitive decline. In a recent study a novel compound, \npoly-N-methylated amyloid beta (Aβ)-peptide C-terminal fragments (MEPTIDES) was shown to \nreduce Aβ toxicity in vitro and in Drosophila melanogaster, however whether this novel drug is \nequally effective in mammals to inhibit Aβ-induced toxicity remains unclear. Accordingly in the \npresent study we investigated the effects of MEPTIDES on the neurotoxicity induced by a single \nintracerebral (i.c.) injection of Aβ42 into the dorsal hippocampus of adult male Sprague-Dawley \n(SD) rats, a model of AD-like impaired learning and memory, and explored the implications of \nthese findings for possible future management therapies or AD.
Author: Siyabonga G. Sibiya
Language: English
Subfield: Cellular and Molecular Neuroscience
Field: Neuroscience
Domain: Life Sciences
Open Access status: green
OpenAlex ID: W2441575946