期刊
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
卷 22, 期 9, 页码 -出版社
MDPI
DOI: 10.3390/ijms22094914
关键词
protein aggregation; amyloid β peptide (Aβ ); toxic oligomers; amyloid fibrils; tau protein; neurodegeneration; ionic dysregulation; glutamatergic receptors; NMDA; AMPA
资金
- University of Florence (Fondi Ateneo)
- Ministry of Education, Universities and Research of Italy (Progetto Dipartimento di Eccellenza Gender Medicine)
Alzheimer's disease is a common age-related neurodegenerative disorder characterized by amyloid beta-protein deposition and neurofibrillary tangles, leading to cognitive decline and dementia. Despite extensive research, the exact mechanisms underlying AD remain unknown and effective treatment is not available.
Alzheimer's disease (AD) is the most common age-related neurodegenerative disorder that is characterized by amyloid beta-protein deposition in senile plaques, neurofibrillary tangles consisting of abnormally phosphorylated tau protein, and neuronal loss leading to cognitive decline and dementia. Despite extensive research, the exact mechanisms underlying AD remain unknown and effective treatment is not available. Many hypotheses have been proposed to explain AD pathophysiology; however, there is general consensus that the abnormal aggregation of the amyloid beta peptide (A beta) is the initial event triggering a pathogenic cascade of degenerating events in cholinergic neurons. The dysregulation of calcium homeostasis has been studied considerably to clarify the mechanisms of neurodegeneration induced by A beta. Intracellular calcium acts as a second messenger and plays a key role in the regulation of neuronal functions, such as neural growth and differentiation, action potential, and synaptic plasticity. The calcium hypothesis of AD posits that activation of the amyloidogenic pathway affects neuronal Ca2+ homeostasis and the mechanisms responsible for learning and memory. A beta can disrupt Ca2+ signaling through several mechanisms, by increasing the influx of Ca2+ from the extracellular space and by activating its release from intracellular stores. Here, we review the different molecular mechanisms and receptors involved in calcium dysregulation in AD and possible therapeutic strategies for improving the treatment.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据