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Guillain–Barré syndrome – nerve damage. Neuroregeneration in the peripheral nervous system (PNS) occurs to a significant degree. [5] [6] After an injury to the axon, peripheral neurons activate a variety of signaling pathways which turn on pro-growth genes, leading to reformation of a functional growth cone and regeneration.
Endogenous regeneration in the brain is the ability of cells to engage in the repair and regeneration process. While the brain has a limited capacity for regeneration, endogenous neural stem cells, as well as numerous pro-regenerative molecules, can participate in replacing and repairing damaged or diseased neurons and glial cells.
The axolotl is less commonly used than other vertebrates, but is still a classical model for examining regeneration and neurogenesis. Though the axolotl has made its place in biomedical research in terms of limb regeneration, [19] [20] the model organism has displayed a robust ability to generate new neurons following damage.
Neurodegenerative diseases include amyotrophic lateral sclerosis, multiple sclerosis, Parkinson's disease, Alzheimer's disease, Huntington's disease, multiple system atrophy, tauopathies, and prion diseases. Neurodegeneration can be found in the brain at many different levels of neuronal circuitry, ranging from molecular to systemic. [4]
Therefore, a potential source of cells for lung regeneration has been found; however, due to advances in inducing stem cells and directing their differentiation, major progress in lung regeneration has consistently featured the use of patient-derived iPSCs and bioscaffolds. The extracellular matrix is the key to generating entire organs in vitro.
The neurons that are able to re-enter the cell cycle are much more likely to undergo apoptosis and lead to the disease phenotypes. In Alzheimer’s disease, affected neurons show signs of DNA replication such as phosphorylated Mcm2 and cell cycle regulators cyclin D, Cdk4, phosphorylated Rb, E2F1, and cyclin E.
The first postmitotic cells must leave the stem cell niche and migrate outward to form the preplate, which is destined to become Cajal–Retzius cells and subplate neurons. These cells do so by somal translocation. Neurons migrating with this mode of locomotion are bipolar and attach the leading edge of the process to the pia.
Neurons are highly oxygenated cells and as a consequence DNA damage caused by chronic exposure to endogenous reactive oxygen species is a substantial challenge for neurons. [8] Germline mutations deficient in the repair of DNA damages cause neuronal dysfunction and are etiologically linked to many neurological disorders. [ 8 ]