Spinal muscular atrophy (SMA) is an autosomal disease caused by deletion or mutation(s) of thesurvival motor neuron 1 (SMN1) gene. A highly homologous gene, SMN2, is present in all patients but yields low levels of the full-length SMN protein.
Our objective is to understand how axonal transport and local protein synthesis contribute to hyperexcitability exhibited by damaged neurons leading to neuropathic pain states.
Oxidative stress is an event associated with a variety of neurological disorders, including stroke. It occurs when neurons are unable to maintain reactive oxygen species (ROS) homeostasis.
The human brain represents only 2% of the body weight but it utilizes around 20% of total body glucose. This shows how crucial glucose metabolism is for the proper functioning of neurons and other cell types in the brain.
Intracerebral hemorrhage (ICH) accounts for about 15% of all strokes and has the highest mortality rates among strokes with up to 50% within 30 days after the insult. It is known to increase intracranial pressure and is associated with excitotoxicity, oxidative stress, and inflammation.
Thiamine (vitamin B1) deficiency (TD) produces a mild, chronic impairment of oxidative metabolism that models the diminished metabolism and reduced activities of the thiamine-dependent mitochondrial enzymes that occur in brain in several common age-related neurodegenerative disorders.
Diminished brain metabolism and oxidative stress are characteristic features of Alzheimer's disease (AD). The mechanisms underlying these changes are as yet poorly defined.
