Neuroscience

Beyond Genes: Treating Memory Loss with Minimum Adverse Effects

By Jamshed Arslan Pharm.D.
Research Associate, University of Alabama, Birmingham

Necroptosis in Health and Disease

PINK1 as a Mitochondrial Health Sensor and Neuroprotector

The Proteasome and Autophagy Pathways in Alzheimer's Disease

The neurodegenerative disorder, Alzheimer's disease, is responsible for 60 to 80% of all dementia cases.1   Neurodegeneration occurs in response to the accumulation of amyloid-β plaques and neurofibrillary tangles composed of hyperphosphorylated tau.

Article Review: Dual effects of carbon monoxide on pericytes and neurogenesis in traumatic brain injury

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

The role of MHC Class II RT1B and immune response post brain injury

The major histocompatibility complex (MHC) is responsible for binding peptide fragments arising from pathogens in order to display them on the cell surface for recognition from immune cells.  Once recognized, the foreign pathogen is typically evaded. The MHC complex is broken into two categories, MHC Class I proteins and MHC Class II proteins.  MHC complex I and II proteins are all very different and contain specific molecules to bind different peptides – in fact, they have been described as the most polymorphic genes there are.

The C99 fragment of amyloid precursor protein (APP)

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

Beta Amyloid (MOAB2) and the link between traumatic brain injury and Alzheimer’s disease

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.

Winter is coming, and TRPM8 welcomes the cold!

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 and neurogenesis

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.

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