Preliminar study of calcium binding proteins in A β-Amyloid iinjected model

Abstract

Alzheimer's disease (AD) is the most common neurodegenerative disease and it is characterized by a progressive cognitive decline with memory loss. Histopathological examination of AD postmortem brains revealed the presence of numerous senile plaques (amyloid plaques) and neurofibrillary tangles (NFT). The administration of Aβ25-35 into the hippocampus is predominantly used in animal studies and has been shown to induce biochemical changes in animals which are similar to what is observed in AD patients. Recent human and preclinical studies have provided convincing evidence that AD is a degenerative metabolic disease, which is mediated by impairments in brain insulin responsiveness, glucose utilization, and energy metabolism.The insulin superfamily comprises the vertebrate insulin, two insulin-like growth factors (IGF1, IGF2), four insulin-like peptides (INSL3, INSL4, INSL5, INSL6), as well as three relaxin peptides (RLN1, RLN2, RLN3). RLN3 accumulation and/or hyperinsulinemia may have similar effects regarding deficient Aβ clearance. Previous data on the distribution of RLN3 fibres in the brain have shown a close correlation with areas that are specially sensitive to AD pathologies including the medial septum, amygdala and hippocampus. Numerous evidences suggest that a deregulation of Ca+2 signaling may play a major role in disease progression. Different proteins, including CB, CR and PV, may offer neuroprotection by maintaining calcium homeostasis. After having conducted the study, we have noticed that the injection of Aβ 25-35 induce the same changes in calcium-binding proteins expression in septum and hippocampus of the contralateral hemisphere.