Neuroscience

Alzheimer’s Disease (AD) is a neurodegenerative disorder that is characterized by an abundance of the beta-amyloid peptide in the brain.  When AD was first discovered, it was determined that beta-amyloid was produced as a result of the proteolysis of the amyloid precursor protein (APP).  Aside from its role in AD, the single-pass transmembrane APP has a high expression level in the brain and tends to concentrate at the synapses of neurons.  Because of this localization, it has been suggested that APP plays a role in synapse formation and potentially plasticity.  However, the

An epidemiological association between traumatic brain injury (TBI) and Alzheimer's disease (AD) has long been established.  Interestingly, an increase in beta amyloid  (one hallmark of AD) directly following TBI has been observed.  In fact, it has been reported that with a greater level of TBI comes a higher risk of developing AD, or other neurodegenerative disorders, in the future.  Roberts et al first presented research that beta amyloid plaques found in TBI patients are very similar to those found in AD patients.

TRPM8, or transient receptor potential melastatin 8, is a nonselective cation channel that is activated by cold environments and menthol-like cooling compounds.  While TRPM8 is best known for its location in peripheral nerve endings, it has functionality both inside and out of the nervous system.  Within the nervous system, TRPM8 is responsible for our response to cold and or menthol like stimuli.  Our reaction to cold sensation is involved in a variety of processes and can be a part of reactions such as asthma.  Outside of the nervous system, TRPM8 has shown high expression in pro

Beta tubulin III, also known as Tuj-1, is a class III member of the beta tubulin protein family. Beta tubulins are one of two structural components that form our microtubule network.

Exosomes are spherical to cup-shaped bilayered membrane enclosed nanosize vesicles (30-100 nm) which have the ability to shuttle active cargoes between cells. Johnstone et al. 1987 pioneered in documenting the generation of exosomes in differentiating reticulocytes as a result of the fusion of multi-vesicular endosomes/MVBs with the plasma membrane.

Tyrosine hydroxylase (TH) is a crucial enzyme involved in the biosynthesis of dopamine, norepinephrine and epinephrine in the brain.

xCT is a sodium independent glutamate transporter that regulates the exchange of extracellular l-cystine and intracellular l-glutamate across the plasma membrane. This process is critical to glutathione production and protection from subsequent oxidative stress.

Niemann-Pick type C1 (NPC1) mediates low-density cholesterol transport from late endosomes and lysosomes to other areas of the cell via receptor mediation endocytosis.  Although cholesterol moves freely inside the cell, it cannot independently export out of the lysosome, which is where NPC1 steps in.

Nogo is a neurite outgrowth inhibitor protein that plays an important role during central nervous system (CNS) development as well as in endoplasmic reticulum signaling regulation. Studies using Nogo antibodies have revealed Nogo proteins regulate precursor migration, neurite growth and branching in the developing CNS. In addition, Nogo serves as a negative regulator of neuronal growth in the adult CNS, causing wiring stabilization but greatly limiting any regeneration abilities (Schwab, 2010).

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.