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Application of nicergoline and gastrodin in synergistic prevention and treatment of Alzheimer's disease (AD)

A technology for Alzheimer's disease and nicergoline, which is applied in the field of small molecule drugs in clinical medicine, can solve problems such as no related reports, and achieve the effect of improving changes in cerebrovascular function.

Inactive Publication Date: 2020-11-27
谭骏
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  • Summary
  • Abstract
  • Description
  • Claims
  • Application Information

AI Technical Summary

Problems solved by technology

[0006] In view of the above, the present invention proves that Nicergoline and gastrodin are used alone or in combination, that is, NTM428 acts on α1-adrenergic receptors by inhibiting β-amyloid protein, thereby improving cerebrovascular function and preventing Or reverse the pathological damage and behavioral disorder of AD model mice, and be used for the prevention and treatment of AD. There is no relevant report about the synergistic prevention and treatment of AD of Nicergoline and gastrodin of the present invention, that is, NTM428

Method used

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Experimental program
Comparison scheme
Effect test

Embodiment 1

[0026] Embodiment 1, the application of Nicergoline and gastrodin synergistically preventing and treating Alzheimer's disease of the present invention, all molecular biological mechanisms and experimental methods that Nicergoline and gastrodin are used alone or in combination are as follows:

[0027] Further, α1-adrenergic receptor activity is elevated in AD patients and mouse AD models

[0028] Including: α1-adrenergic receptor activity is elevated in AD patients;

[0029] α1-adrenoceptor-mediated activation of G protein in the brains of APP / PS1 mice was increased compared with non-transgenic mice of the same age, and in 6.5-month-old APP / PS1 mice, α1-adrenergic receptors body-induced increased cerebral vasoconstrictor responses, no difference in α1-adrenoceptor-mediated G protein activation or α1-adrenoceptor density between 4-week-old APP / PS1 mice and non-transgenic mice, showed that changes in the response efficiency of α1-adrenergic receptors in 6.5-month-old transgenic ...

Embodiment 2

[0038] Embodiment 2, the application of Nicergoline and gastrodin synergistically preventing and treating Alzheimer's disease of the present invention, all molecular biological mechanisms and experimental methods that Nicergoline and gastrodin are used alone or in combination are as follows:

[0039] Further, α1-adrenergic receptor activity is elevated in AD patients and mouse AD models

[0040] Including: α1-adrenergic receptor activity is elevated in AD patients;

[0041] α1-adrenoceptor-mediated activation of G protein in the brains of APP / PS1 mice was increased compared with non-transgenic mice of the same age, and in 5-month-old APP / PS1 mice, α1-adrenergic In vivo-induced increased cerebral vasoconstrictor responses, no difference in α1-adrenergic receptor-mediated G protein activation or α1-adrenoceptor density between 3-week-old APP / PS1 mice and non-transgenic mice, showed that changes in the response efficiency of α1-adrenergic receptors in 5-month-old transgenic mice...

Embodiment 3

[0050] Embodiment 3, the application of Nicergoline and gastrodin synergistically preventing and treating Alzheimer's disease of the present invention, all molecular biological mechanisms and experimental methods that Nicergoline and gastrodin are used alone or in combination are as follows:

[0051] Further, α1-adrenergic receptor activity is elevated in AD patients and mouse AD models

[0052] Including: α1-adrenergic receptor activity is elevated in AD patients;

[0053] α1-adrenoceptor-mediated activation of G protein in the brains of APP / PS1 mice was increased compared with non-transgenic mice of the same age, and in 9-month-old APP / PS1 mice, α1-adrenergic receptors body-induced increased cerebral vasoconstrictor responses, no difference in α1-adrenoceptor-mediated G protein activation or α1-adrenoceptor density between 7-week-old APP / PS1 mice and non-transgenic mice, showed that changes in the response efficiency of α1-adrenergic receptors in 9-month-old transgenic mice...

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PUM

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Abstract

The invention discloses application of nicergoline and gastrodin in synergistic prevention and treatment of Alzheimer's disease (AD), and relates to the field of clinical medical small molecule drugs.The nicergoline and the gastrodin are obtained by inhibiting beta-amyloid oligopeptide mediated [alpha]1-adrenergic receptor chronic activation-like cerebrovascular function change, AD-like pathological change and preclinical research of cognitive impairment for natural small molecular compounds; according to the application in preventing and treating AD, in the application of prevention and treatment of the AD, it is proved from the molecular, cellular and animal levels that the nicergoline and the gastrodin are independently used or jointly used for inhibiting beta-amyloid oligopeptide mediated [alpha]1-adrenergic receptor chronic activation-like cerebrovascular smooth muscle cell molecular signaling pathways and cerebrovascular tissue activity, and improving cerebrovascular function change and AD-like molecular pathological damage and behavioral disorder of AD model mice.

Description

technical field [0001] The invention relates to the field of small molecule drugs in clinical medicine, in particular to the application of nicergoline and gastrodin in synergistic prevention and treatment of Alzheimer's disease. Background technique [0002] As we all know, Alzheimer's Disease (AD), also known as senile dementia, is a progressive degenerative disease of the central nervous system, mainly manifested in patients with progressive memory impairment, cognitive impairment, and language impairment. , personality loss of control and other behavioral symptoms, commonly known as "old children" and "living dead", seriously affect the life and social functions of patients, and seriously affect the quality of life of patients and close relatives. The etiology and pathogenesis of AD are not yet clear, and the characteristic pathological changes are Extracellular senile plaques by β-amyloid deposition and intracellular neurofibrillary tangles and neuronal loss by hyperpho...

Claims

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Application Information

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IPC IPC(8): A61K31/48A61K31/7034A61P25/28
CPCA61K31/48A61K31/7034A61P25/28A61K2300/00
Inventor 谭骏李崧訾聃谢非非
Owner 谭骏
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