Abstract
Neuropeptide Y (NPY) is a neurotransmitter or neuromodulator that mainly exists in the nervous system. It plays a neuroprotective role in organisms and widely participates in the regulation of various physiological processes in vivo. Studies in both humans and animal models have been revealed that NPY levels are altered in some neurodegenerative and neuroimmune disorders. NPY plays various roles in these diseases, such as exerting a neuroprotective effect, increasing trophic support, decreasing excitotoxicity, regulating calcium homeostasis, and attenuating neuroinflammation. In this review, we will focus on the roles of NPY in the pathological mechanisms of neurodegenerative and neuroimmune diseases, highlighting NPY as a potential therapeutic target in these diseases.
Highlights
Neuropeptide Y (NPY) is a polypeptide composed of 36 amino acid residues, and belongs to the NPY family of neuroendocrine peptides, which includes peptide YY and pancreatic polypeptide
Croce et al (2013) pre-incubated primary rat cortical neurons with NPY and exposed them to Aβ25–35 fragments. They found that NPY mediated a decrease in miR-30a-5p expression and an increase in brain derived neurotrophic factor (BDNF) messenger ribonucleic acids (mRNAs) and protein levels, which possibly contributed to the neuroprotective effect of NPY in rat cortical neurons exposed to amyloid β (Aβ) (Croce et al, 2013)
The results showed that the proliferation of neural precursor cells in the sub-granular zone of the hippocampus increased significantly without further differentiation into neurons
Summary
Neuropeptide Y (NPY) is a polypeptide composed of 36 amino acid residues, and belongs to the NPY family of neuroendocrine peptides, which includes peptide YY and pancreatic polypeptide. NPY plays an important regulatory role in the immune function and inflammatory response of the central nervous system (CNS) such as modulation of chemotaxis of immune cells, phagocytosis, and production and release of cytokines (Ferreira et al, 2010). They found that NPY mediated a decrease in miR-30a-5p expression and an increase in brain derived neurotrophic factor (BDNF) mRNA and protein levels, which possibly contributed to the neuroprotective effect of NPY in rat cortical neurons exposed to Aβ (Croce et al, 2013).
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