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Neuroscience

How to switch from apoptotic to necroptotic cell death? Answer: Autophagy!

By Christina Towers, PhD.

Autophagy’s Paradoxical Role in ALS

Autophagy as a Therapeutic Target: The Double-edged Sword

Polyglutamine Tracts as Autophagy Regulators

Beyond Genes: Treating Memory Loss with Minimum Adverse Effects

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.

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