Optogenetics: implications for Alzheimer’s disease research and therapy

被引:0
作者
Parsa Mirzayi
Parnian Shobeiri
Amirali Kalantari
George Perry
Nima Rezaei
机构
[1] Tehran University of Medical Sciences (TUMS),School of Medicine
[2] Children’s Medical Center Hospital,Network of Immunity in Infection, Malignancy and Autoimmunity (NIIMA)
[3] Universal Scientific Education and Research Network (USERN),Non–Communicable Diseases Research Center, Endocrinology and Metabolism Population Sciences Institute
[4] Tehran University of Medical Sciences,Research Center for Immunodeficiencies, Pediatrics Center of Excellence, Children’s Medical Center
[5] Tehran University of Medical Sciences,Department of Biology and Neurosciences Institute
[6] University of Texas at San Antonio (UTSA),Department of Immunology, School of Medicine
[7] Tehran University of Medical Sciences,Research Center for Immunodeficiencies
[8] Children’s Medical Center,undefined
来源
Molecular Brain | / 15卷
关键词
Alzheimer’s disease; Optogenetics; Neural circuits; Neurodegeneration; Synapse; Molecular pathways; Memory;
D O I
暂无
中图分类号
学科分类号
摘要
Alzheimer’s disease (AD), a critical neurodegenerative condition, has a wide range of effects on brain activity. Synaptic plasticity and neuronal circuits are the most vulnerable in Alzheimer’s disease, but the exact mechanism is unknown. Incorporating optogenetics into the study of AD has resulted in a significant leap in this field during the last decades, kicking off a revolution in our knowledge of the networks that underpin cognitive functions. In Alzheimer's disease, optogenetics can help to reduce and reverse neural circuit and memory impairments. Here we review how optogenetically driven methods have helped expand our knowledge of Alzheimer's disease, and how optogenetic interventions hint at a future translation into therapeutic possibilities for further utilization in clinical settings. In conclusion, neuroscience has witnessed one of its largest revolutions following the introduction of optogenetics into the field.
引用
收藏
相关论文
共 803 条
[51]  
Ayata C(1993)Aß facilitates LTD at Schaffer collateral synapses preferentially in the left hippocampus Nature 358 617-2806
[52]  
Bernstein JG(2008)Spatial sequence coding differs during slow and fast gamma rhythms in the hippocampus Front Neurosci 30 111-792
[53]  
Boyden ES(2003)Temporal encoding of place sequences by hippocampal cell assemblies Philos Trans R Soc Lond B 225 935-1902
[54]  
Zhang F(2007)Heightened synaptic plasticity of hippocampal CA1 neurons during a cholinergically induced rhythmic state Trends Neurosci 416 535-1289
[55]  
Gradinaru V(2020)Relationship of hippocampal theta and gamma oscillations to potentiation of synaptic transmission Brain Struct Funct 924 133-88.e3
[56]  
Adamantidis AR(2002)The discovery of long-term potentiation Nature 14 837-7717
[57]  
Durand R(2002)Hippocampal long-term depression: master or minion in declarative memory processes? Brain Res 18 7-336
[58]  
Airan RD(2008)Dissociation of somatostatin and parvalbumin interneurons circuit dysfunctions underlying hippocampal theta and gamma oscillations impaired by amyloid β oligomers in vivo Nat Med 36 295-314
[59]  
de Lecea L(2020)Naturally secreted oligomers of amyloid beta protein potently inhibit hippocampal long-term potentiation in vivo BMC Biol 22 1363-11857
[60]  
Obi-Nagata K(2013)Soluble oligomers of β amyloid (1–42) inhibit long-term potentiation but not long-term depression in rat dentate gyrus Annu Rev Neurosci 23 199-55