20(S) -protopanaxadiol针对大脑丰富的腺酸酶5来通过调节海马神经可塑性来改善认知功能
Feiyan Chen1, Wenjing Zhang2, Haixia You3
1Research and Experiment Center, School of Chinese Medicine, Nanjing University of Chinese Medicine, Nanjing 210023, China.
概括
腺酸酶5 (AK5) 对认知功能和神经可塑性至关重要. 通过向AK5,20S-protopanaxadiol (PPD) 改善了认知障碍,突出了AK5作为治疗点.
科学领域:
- 神经科学是一个神经科学.
- 药理学 药理学是指药理学的学科.
- 生物化学 生化学
背景情况:
- 人参是一种用于认知障碍的营养补充剂,但其机制尚不清楚.
- 腺酸酶5 (AK5) 被确定为20(S) - - 质原二醇 (PPD) 的标,PPD增加了AK5的活性.
研究的目的:
- 探索PPD如何通过AK5和相关的神经可塑性改善认知障碍.
- 研究AK5在认知功能中的作用和PPD的治疗潜力.
主要方法:
- 已建立的d-银糖诱导的小鼠模型和使用AAV-shRNA-AK5.5的AK5敲击.
- 通过行为测试评估学习和记忆.
- 量化AK5活动,表达 (mRNA,蛋白质) 和海马突触可塑性/神经发生.
主要成果:
- 在小鼠中,AK5的淘汰导致认知障碍和降低海马神经可塑性,反映了d-银糖的影响.
- 在d-银糖诱导的小鼠中,PPD治疗部分恢复了AK5活动/表达,并改善了神经可塑性.
- 由于AK5被淘汰,PPD的认知效益被废除了,这证实了AK5的关键作用.
结论:
- AK5在介导神经可塑性和认知功能方面发挥着至关重要的作用.
- AK5是PPD治疗的关键治疗标,以缓解认知障碍.
- 提高认知能力的PPD机制包括增强AK5活动和神经可塑性.
更多相关视频
相关概念视频
Cognitive Enhancers: Cholinesterase Inhibitors and NMDA Receptor Antagonists
512
Cognitive enhancers, also known as "smart drugs," are substances used to enhance memory, mental alertness, and concentration. These can be natural or synthetic and improve cognition in conditions like Alzheimer's disease (AD) and other neurodegenerative diseases. Some common examples include caffeine, amphetamines, methylphenidate, modafinil, arecoline, donepezil, vortioxetine, and piracetam. These enhancers work on the principle of synaptic plasticity and altered circuit function.
512
Alzheimer's Disease: Treatment
752
Alzheimer's Disease (AD), a neurodegenerative disorder, is pathologically identified by amyloid plaques and neurofibrillary tangles composed of tau protein. AD pharmacotherapy aims to manage cognitive symptoms, delay disease progression, and treat behavioral symptoms. The treatment is primarily symptomatic and palliative, with no definitive disease-modifying therapy available. Cholinesterase inhibitors, including donepezil (Aricept), rivastigmine (Exelon), and galantamine (Razadyne), are...
752
Alzheimer's Disease: Overview
1.6K
Alzheimer's Disease (AD) is a continually advancing neurodegenerative disorder, distinguished by escalating memory loss, cognitive dysfunction, and dementia. The disease unfolds in three stages: preclinical, mild cognitive impairment (MCI), and dementia. Its onset is insidious, and the progression gradual, with the cause not well explained by other disorders.
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ...
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ...
1.6K
Drugs Affecting Neurotransmitter Synthesis
2.1K
Drugs affecting neurotransmitter synthesis can impact the adrenergic neuron and the synthesis of neurotransmitters. For example, α-methyltyrosine and carbidopa target specific enzymes involved in catecholamine synthesis. α-methyltyrosine inhibits the enzyme tyrosine hydroxylase, which converts tyrosine into dopamine. By blocking this enzyme, α-methyltyrosine reduces dopamine production and other catecholamines. Carbidopa, on the other hand, inhibits the enzyme dopa decarboxylase,...
2.1K
Drugs Affecting Neurotransmitter Release or Uptake
1.5K
Certain drugs can affect how neurotransmitters called catecholamines, are released or taken back up in the adrenergic neuron. They can have different effects on the body's sympathetic transmission. Reserpine, a natural compound found in the Rauwolfia shrub, blocks a transporter called vesicular monoamine transporter (VMAT), which leads to a buildup of catecholamines in the cell and reduces sympathetic transmission. Another drug called guanethidine works in multiple ways, including blocking...
1.5K
Long-term Depression
3.0K
Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
Calcium Ion Concentration Mechanism
If over...
Calcium Ion Concentration Mechanism
If over...
3.0K


