Protective potential of glucagon like peptide 2 (GLP-2) against the neurodegeneration

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Neurodegeneration consists in loss of neuron specific types, patt and distribution, leading to progressive dysfunctions of the central ner-vous system. Neurodegenerative diseases include diverse pathological conditions, among which Alzheimer’s and Parkinson’s diseases are the most prevalent ones. Alzheimer’s disease is known as a growing demen-tia, characterized by progressive language, memory, and cognitive loss, while Parkinson’s disease is primarily characterized as a motor disorder. Senile plaques, caused by amyloid β peptide, hyperphosphorylated tau-based neurofibrillary tangles and synapse loss, are the principal patho-logical hallmarks of Alzheimer’s disease. Amyloid β oligomer formation is associated with development of reactive oxygen and nitrogen species, inflammation, calcium-dependent excitotoxicity, impairment of cellular respiration, and alteration of synaptic functions related with leing and memory. Parkinson’s disease is produced by dopaminergic neuron deterioration in the extrapyramidal tract of the midbrain. Accumula-tion of α-synuclein proteins (Lewy bodies) in the central, autonomic, and peripheral nervous system is the hallmark of the Parkinson’s dis-ease. The Levy bodies break the neuronal membrane leading to neu-ronal death through oxidative stress, excitotoxicity, energy failure and neuroinflammation.
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