z-logo
open-access-imgOpen Access
Novel therapeutic targets for amyotrophic lateral sclerosis
Author(s) -
Gitika Batra,
Manav Jain,
Rahul Singh,
Amit Sharma,
Ashutosh Singh,
Ajay Prakash,
Bikash Medhi
Publication year - 2019
Publication title -
indian journal of pharmacology/˜the œindian journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.286
H-Index - 59
eISSN - 1998-3751
pISSN - 0253-7613
DOI - 10.4103/ijp.ijp_823_19
Subject(s) - amyotrophic lateral sclerosis , neuroscience , excitotoxicity , disease , microglia , medicine , motor neuron , neurodegeneration , sod1 , spinal cord , glutamate receptor , biology , inflammation , pathology , immunology , receptor
Amyotrophic lateral sclerosis (ALS) is an untreatable and fatal neurodegenerative disease that is identified by the loss of motor neurons in the spinal cord, brain stem, and motor cortex which theatrically reduces life expectancy. Although the primary cause of ALS remains unclear, its heterogeneity put forward for consideration of association with various factors, including endogenous and/or environmental ones, which may be involved in progressive motor neuron stress that causes activation of different cell death pathways. It is hypothesized that this disease is triggered by factors related to genetic, environmental, and age-dependent risk. In spite of large neurobiological, molecular and genetic research, at the beginning of the 21 st century, ALS still remains one of the most devastating neurodegenerative diseases because of the lack of effective therapeutic targets. It is a challenge for the clinical and scientific community. A better understanding of the etiology of ALS is necessary to develop specific targets of this progressive neurodegenerative disease. This review states about the current knowledge of targets in ALS research. This review provides an overview of the contribution of different targets like mitochondrial dysfunction, glutamate transport and excitotoxicity, protein accumulation, Oxidative stress, neuromuscular junction, microglia, and other molecular targets in the pathogenesis of ALS.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.
Having issues? You can contact us here