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A neuron observed under an optical microscope. Neuroprotection refers to the relative preservation of neuronal structure and/or function. [1] In the case of an ongoing insult (a neurodegenerative insult) the relative preservation of neuronal integrity implies a reduction in the rate of neuronal loss over time, which can be expressed as a differential equation.
Factors such as myelin debris, which is formed by the injury at the damage site, has been shown to induce the phenotype shift from M2 to M1. [19] A decreased population of M2 macrophages and an increased population of M1 macrophages is associated with chronic inflammation. [19] Short-term inflammation is important in clearing cell debris from ...
The increase in protein within the neuron leads to this change in the cytoskeleton. For example, there is an increase in phosphorylated neurofilament proteins and cytoskeletal components, tubulin and actin, in neurons undergoing chromatolysis. [4] The increase in protein can be explained by the increase in cytoskeleton size.
Phagocytic microglia travel to the site of the injury, engulf the offending material, and secrete pro-inflammatory factors to promote more cells to proliferate and do the same. Activated phagocytic microglia also interact with astrocytes and neural cells to fight off any infection or inflammation as quickly as possible with minimal damage to ...
Molecular neuroscience is a branch of neuroscience that observes concepts in molecular biology applied to the nervous systems of animals. The scope of this subject covers topics such as molecular neuroanatomy, mechanisms of molecular signaling in the nervous system, the effects of genetics and epigenetics on neuronal development, and the molecular basis for neuroplasticity and ...
These include destabilizing changes in the primary amino acid sequence of the protein, post-translational modifications (such as hyperphosphorylation), changes in temperature or pH, an increase in production of a protein, or a decrease in its clearance. [1] [5] [15] Advancing age is a strong risk factor, [1] as is traumatic brain injury.
Nerve growth factor (NGF) typically has a low level of expression in nerves that are healthy and not growing or developing, but in response to nerve injury NGF expression increases in Schwann cells. This is a mechanism to increase growth and proliferation of Schwann cells at the distal stump in order to prepare for reception of the regenerating ...
MAO-B levels have been found to increase with age, suggesting a role in natural age related cognitive decline and the increased likelihood of developing neurological diseases later in life. [20] More active polymorphisms of the MAO-B gene have been linked to negative emotionality , and suspected as an underlying factor in depression . [ 21 ]