Evaluating a new drug to combat Alzheimer's disease.

Abstract

Alzheimer’s disease (AD), a progressive neurodegenerative disorder that affects mostly the limbic system and the neocortical areas of the brain, is the most prevalent form of dementia affecting the elderly population. Twenty-nine million people live with the disease worldwide, 10% of the population > 65 years of age and 50 % of the population > 85 years of age. These figures are expected to increase exponentially over the next few decades and reach 81.1 million by the year 2040. Hallmark lesions include extracellular deposition of β-amyloid protein (Aβ) fibrillar plaques and intraneuronal neurofibrillary tangles (NFTs), which impair synaptic plasticity in the target regions of the brain thereby producing a progressive decline in cognitive function, with the earliest signs observed in learning and memory. Current therapies of AD are merely palliative and only slow down cognitive decline. In a recent study a novel compound, poly-N-methylated amyloid beta (Aβ)-peptide C-terminal fragments (MEPTIDES) was shown to reduce Aβ toxicity in vitro and in Drosophila melanogaster, however whether this novel drug is equally effective in mammals to inhibit Aβ-induced toxicity remains unclear. Accordingly in the present study we investigated the effects of MEPTIDES on the neurotoxicity induced by a single intracerebral (i.c.) injection of Aβ42 into the dorsal hippocampus of adult male Sprague-Dawley (SD) rats, a model of AD-like impaired learning and memory, and explored the implications of these findings for possible future management therapies or AD.