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Amyotrophic lateral sclerosis (ALS) is a fatal motor neuron disease (MND) characterised 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 included 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% beyond 10 years of age. 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, current review specially
targeted in the investigation of clinical and pre-clinical features available for ALS to understand the pathogenic
mechanisms and to explore the pharmacological interventions associated with up-regulation of intracellular adenyl
cyclase/cAMP/CREB and mitochondrial-ETC coenzyme-Q10 activation as a future drug target in the amelioration of
ALS mediated motor neuronal dysfunctions.
“Cardiac Specific Adenyl Cyclase Type 8 Overexpression Induces Chronic Cardiac Exercise and Leads to a Unique Form of Cardiac Growth.”
