Application of CART (Cocaine Amphetamine Regulated Transcript) in preparing medicaments for treating alzheimers diseases

Abstract

The invention relates to application of CART (Cocaine Amphetamine Regulated Transcript) in preparing medicaments for treating alzheimers diseases. In the invention, CART is prepared into injection preparations for treating alzheimers diseases, and the defects of the traditional medicaments for enhancing cholinergic action and N-methyl-D-aspartic acid (NMDA) receptor antagonists are overcome. The novel medicament has multiple target point actions on the generation and the degradation of A beta as well as the influence of the neurotoxicity and the molecular mechanism of the A beta. The invention has effects on effectively treating dementia with estrogen and up-regulating intracephalic CART; more CARTs are distributed in intracephalic hippocampus; CART exists in intracephalic acetylcholine neurons and can promote the release of acetylcholine; and mitochondrial dysfunction induced by A beta neurotoxicity is the main pathway for the A beta to cause neuronal apoptosis. The CART has a directaction on mitochondrial succinodehydrogenase subunit B and can maintain the respiration of mitochondria and the generation of energy, alleviate oxidative stress, stabilize mitochondrial membrane potential and prevent the mitochondria from being damaged, thereby inhibiting apoptosis.

Description

technical field The invention relates to the application of a medicine, in particular to the application of a small molecular neuropeptide cocaine-amphetamine-regulated transcription peptide (cocaine and amphetamine-regulated transcript, referred to as CART) as a medicine for treating Alzheimer's disease. Background technique Alzheimer's disease (AD) is the most common neurodegenerative disease and the most common cause of senile dementia, manifested as progressive mental decline. The crowd prevalence rate over 65 years old has reached 5-10%, and the crowd prevalence rate over 85 years old has reached 20%-40%. The main pathological mechanism is that Aβ deposits inside and outside the nerve cells of the brain, leading to the death of nerve cells. Aβ is derived from its precursor protein (amyloid precursor protein, APP). APP in the brain is cleaved by β-site APP-cleavingenzymel (BACE1) to produce sAPPβ and C99, and then cleaved by γ-secretase to produce Aβ40 or Aβ42. Among t...

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Problems solved by technology

However, the excitotoxicity caused by NMDA receptor activation is involved in the pathological process of brain injury

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