Affiliation:
1. Department of Pharmacology, ISF College of Pharmacy, Moga-142001, Punjab, India
Abstract
Amyotrophic lateral sclerosis (ALS) is a fatal motor neuron disease (MND) characterized
by the death of upper and lower motor neurons (corticospinal tract) in the motor cortex, basal
ganglia, brain stem, and spinal cord. The patient experiences the sign and symptoms between 55 to
75 years of age, which include impaired motor movement, difficulty in speaking and swallowing,
grip loss, muscle atrophy, spasticity, and sometimes associated with memory and cognitive impairments.
Median survival is 3 to 5 years after diagnosis and 5 to 10% of the patients live for more
than 10 years. The limited intervention of pharmacologically active compounds, that are used clinically,
is majorly associated with the narrow therapeutic index. Pre-clinically established experimental
models, where neurotoxin methyl mercury mimics the ALS like behavioural and neurochemical
alterations in rodents associated with neuronal mitochondrial dysfunctions and downregulation of
adenyl cyclase mediated cAMP/CREB, is the main pathological hallmark for the progression of
ALS in central as well in the peripheral nervous system. Despite the considerable investigation into
neuroprotection, it still constrains treatment choices to strong care and organization of ALS complications.
Therefore, this current review specially targeted the investigation of clinical and pre-clinical
features available for ALS to understand the pathogenic mechanisms and to explore the pharmacological
interventions associated with the up-regulation of intracellular adenyl cyclase/cAMP/
CREB and activation of mitochondrial-ETC coenzyme-Q10 as a future drug target in the amelioration
of ALS mediated motor neuronal dysfunctions.
Publisher
Bentham Science Publishers Ltd.
Subject
General Health Professions
Cited by
9 articles.
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