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您的检索式：作者名="Eran Perlson"
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| 1 | Phosphatidylserine improves axonal transport by inhibition of HDAC and has potential in treatment of neurodegenerative diseases显示文摘Familial dysautonomia(FD) is a rare children neurodegenerative disease caused due to a point mutation in the IKBKAP gene that results in decreased IKK complex-associated protein(IKAP) protein production. The disease affects mostly the dorsal root ganglion(DRG) and the sympathetic ganglion. Recently, we found that the molecular mechanisms underlying neurodegeneration in FD patients are defects in axonal transport of nerve growth factors and microtubule stability in the DRG. Neurons are highly polarized cells with very long axons. In order to survive and maintain proper function, neurons depend on transport of proteins and other cellular components from the neuronal body along the axons. We further demonstrated that IKAP is necessary for axon maintenance and showed that phosphatidylserine acts as an HDAC6 inhibitor to rescue neuronal function in FD cells. In this review, we will highlight our latest research findings. | Shiran Naftelberg Gil Ast Eran Perlson | 2017 | Neural Regeneration Research2017，12，4： | 2 |
| 2 | Receptor-mediated increase in rabies virus axonal transport显示文摘Rabies virus(RABV)of the rhabdoviridae family is a prototype neurotropic virus that causes a fatal disease,and is still a major risk mostly in developing countries.A key step in the RABV infection process is its arrival into the central nervous system(CNS),for which it uses the cellular transport machinery.Neurons are irregular cells with a specialized anatomy,and often extend lengthy axons that may span over a meter long.In infected organisms,RABV virions enter the neuron periphery at the area of a bite and must overcome great distances in | Shani Gluska Stefan Finke Eran Perlson | 2015 | Neural Regeneration Research2015，10，6： | 0 |
| 3 | Neuromuscular junction mitochondrial enrichment: a “double-edged sword” underlying the selective motor neuron vulnerability in amyotrophic lateral sclerosis显示文摘Motor neurons are highly polarized cells,with long axons that extend to more than 1 m in the adult human.The axons further arborize into a specialized synaptic compartment,the motor unit,containing up to 2000 neuromuscular junctions(NMJs).While the size of other neuronal synapses can be up to 1μm,the NMJ is much larger and can reach 10–30μm(Jones et al.,2017).The vast size of the motor unit requires motor neurons to evolutionally adapt and supply this distal portion with a sufficient amount of ATP,as well as to replenish the axonal protein pool in order to maintain their synapses. | Topaz Altman Eran Perlson | 2021 | Neural Regeneration Research2021，16，1： | 0 |
| 4 | Muscle secretion of toxic factors,regulated by miR126-5p,facilitates motor neuron degeneration in amyotrophic lateral sclerosis显示文摘Amyotrophic lateral sclerosis(ALS)is a lethal neurodegenerative disease characterized by neuromuscular junction(NMJ)disruption,motor neuron(MN)axon degeneration,and neuronal death.Unfortunately,there is currently no effective treatment available for ALS and consequently,most patients die several years post diagnosis.The neurodegeneration that occurs in ALS is considered to be a non-cell autonomous process involving interactions between the motor neuron and its diverse extracellular microenvironments via an unknown mechanism.Distal Axonopathy is one of the early disease signs;however,the involvement and contribution of neighboring tissues and specifically,the muscle environment to the disease pathology remain controversial.Few works have concluded that muscles play a minor role or none at all in ALS pathology. | Roy Maimon Eran Perlson | 2019 | Neural Regeneration Research2019，14，6： | 0 |
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