Traumatic brain injury (TBI) currently contributes to nearly 30% of all injury deaths in the United States. Characterized by an abrasive head injury that interrupts normal brain function, TBI can range from mild to severe. Mild symptoms can present themselves as excessive tiredness, difficulty concentrating and lack of clear thinking. Severe cases of TBI are hallmarked by unusual behavior, seizures and loss of consciousness. Research has shown that on a molecular level TBI triggers various mechanisms of cell death alongside attempted tissue recovery, therefore Choi et al sought
Synapsins are a family of neuronal proteins that are most renowned for their activity in modulating the pre-synaptic terminal. Synapsin’s behavior is regulated by protein kinases and phosphatases, which alter the way that synapsin’s interact with actin filaments and other nearby proteins. There are three isoforms of Synapsin – Synapsin I, II and III. Synapsin I specifically localizes to the membrane of presynaptic vesicles and plays a role in regulation of axonogenesis and synaptogenesis.
GFAP, a class-III intermediate filament, is a 50kDa protein which is found in the mature and developing astrocytes in the CNS, non-myelinating Schwann cells in the PNS, enteric glial cells (enteric nervous system/ENS), ependymal cells, and radial glia of the developing brain.
Clinical depression (also known as major depressive disorder or MDD) affects many people, but the biological processes that cause it (and are influenced by its treatments) are not well understood. Adult neurogenesis is a newly emerging field that could contribute to our knowledge of the etiology of depression and the effects of antidepressants. Nestin antibodies are key tools for this research, as they can be used to identify developing neurons.