Chemical surface modification of neuron-surface interfaces is essential for the development of biologically active and functional neural interfaces.
The 662 genes associated with the modification of 128Q-neuron dysfunction appeared to encompass a variety of biological processes (cell death, protein folding, intracellular transport, metabolic processes, response to stress, stress-activated pathways) that may have a role in neurodegenerative disease pathogenesis as suggested by their functional classification using GO annotations.
We use a modification of Rinzel's neuron model [31] presented by Rubin [32] with synaptic coupling [32].
Together, a pathway that is critical for neuron differentiation is established, and modification of hMSCs to accelerate neuron differentiation may have important clinical implications in the regeneration of CNS repair of injured brain and spinal cord.
This modification of hMSCs to accelerate neuron differentiation may have important clinical implication in the regeneration of neurodegenerative diseases.
Evidence is accumulating that the control of gene transcription through epigenetic modification of chromatin structure in neurons has an important role in cognitive processes and in the etiology of ID.
Continuous and intense nociceptive input from the OA knee joint may drive central sensitization, which may arise from chronic nociceptor stimulation and subsequent modification of central pain-transmitting neurons, and may be clinically associated with NP qualities [ 1, 2].
Taken together these considerations let us to conclude that the reduction of the incubation period we observed in mice treated with IL-12 and IL-18 is not explainable by modification of PrPC expression in neurons; however we can not exclude that IL-12 and IL-18-activated microglia overexpress PrPC, as it is true for IFN-γ-activated human CD14+ monocytes [ 43].
Neurons with similar FSIs are more likely to be functionally connected, but the degree of feature selectivity is subject to substantial modification by target neuron processing.
The slow modification of the connectivity between the neurons is commonly thought to be the essence of learning.
Proposed mechanisms include neuromodulatory effects on different enzymes and secondly on amino acids and the selective modification of the function of epileptic neurons [ 26 ].
