Evaluation of Neuroprotective and Neuroregenerative Potential of NeuroAiD™ II(MLC901) in a Rat Model of Kainic Acid-Induced Spinal Cord Injury.

Excitotoxic damage caused by high extracellular levels of glutamate in the spinal cord results in neuronal loss and severe locomotor impairment. This study investigates the efficacy of NeuroAiD II (MLC901), an herbal formulation, in promoting nerve regeneration following spinal cord injury (SCI) induced by kainic acid (KA). KA, a potent glutamate receptor agonist, causes excitotoxic damage in the spinal cord, leading to neuronal loss and locomotor impairment.

Profiling of autoantibodies in the sera of glioblastoma patients.

This study aimed to determine the expression pattern of autoantibody proteins from the serum of grade IV glioblastoma patients. We performed high throughput antibody profiling via the Sengenics i-Ome Protein Array to determine the differentially expressed autoantibodies. The results portrayed that anti-COL4A3BP and anti-HSP90AA1 were among the upregulated autoantibodies in glioblastoma sera.

NeuroAiD-II (MLC901) Promoted Neurogenesis by Activating the PI3K/AKT/GSK-3β Signaling Pathway in Rat Spinal Cord Injury Models.

Traumatic damage to the spinal cord (SCI) frequently leads to irreversible neurological deficits, which may be related to apoptotic neurodegeneration in nerve tissue. The MLC901 treatment possesses neuroprotective and neuroregenerative activity. This study aimed to explore the regenerative potential of MLC901 and the molecular mechanisms promoting neurogenesis and functional recovery after SCI in rats.

Mechanical scratch injury on differentiated motor neuron of NSC-34 cells as an in vitro model for evaluation of neuroregeneration potential of NeuroAiD II (MLC901).

Background: Spinal cord regeneration is considered an ultimate achievement in the field of neuroscience. In vitro, neural stem cell (NSC-34) motor neuron-like cell cultures are powerful tools to study specific molecular pathways involved in neurogenesis.

Purpose: We aimed to demonstrate the usefulness of the in vitro injury model using the mechanical scratch method and to evaluate the effect of MLC901 in injured neuronal cells.

Protocol paper: kainic acid excitotoxicity-induced spinal cord injury paraplegia in Sprague-Dawley rats.

Background: Excitotoxicity-induced in vivo injury models are vital to reflect the pathophysiological features of acute spinal cord injury (SCI) in humans. The duration and concentration of chemical treatment controls the extent of neuronal cell damage. The extent of injury is explained in relation to locomotor and behavioural activity.

Effects of Different Scan Duration on Brain Effective Connectivity among Default Mode Network Nodes.

Background: Resting-state functional magnetic resonance imaging (rs-fMRI) can evaluate brain functional connectivity without requiring subjects to perform a specific task. This rs-fMRI is very useful in patients with cognitive decline or unable to respond to tasks. However, long scan durations have been suggested to measure connectivity between brain areas to produce more reliable results, which are not clinically optimal.

Spinal Cord Injury: Pathophysiology, Multimolecular Interactions, and Underlying Recovery Mechanisms.

Spinal cord injury (SCI) is a destructive neurological and pathological state that causes major motor, sensory and autonomic dysfunctions. Its pathophysiology comprises acute and chronic phases and incorporates a cascade of destructive events such as ischemia, oxidative stress, inflammatory events, apoptotic pathways and locomotor dysfunctions. Many therapeutic strategies have been proposed to overcome neurodegenerative events and reduce secondary neuronal damage.