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MiR-29 has multiple targets that may affect neuronal growth (Govek et al., 2005; Wang et al., 2013).
In addition, the release of numerous cytokines, including interleukin-1β (IL-1β), IL-6, and tumor necrosis factor α (TNF-α) [41], activates the immune system which, in turn, may affect neuronal function and increase pain responses.
Neuronal damage (reflected in altered WM structure) may affect neuronal signal transfer and, thus, cognition (35).
We also hypothesized that α-synuclein may affect neuronal survival in a non-cell autonomous manner by triggering inflammation.
Finally, a genetic screen for M1-defective phenotypes identified nine mutations for M1 development, including a mutation that may affect neuronal differentiation or cell fate specification.
However, this is an indirect measure because incorrect patterning and morphogenesis of other tissues may affect neuronal migration and, thus, correct positioning.
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While neurological dysfunction in patients with tuberous sclerosis is clearly linked to structural brain abnormalities in the central nervous system [1], recent work has provided evidence that TSC1/2 may affect neural development by altering neuronal morphology and function.
Various lines of evidence suggest that sleep disorders may negatively affect neuronal plasticity and cognitive function.
These results suggest that 5-HT depletion may adversely affect neuronal survival following intrastriatal QA exposure and lend support to the hypothesis that increasing 5-HT levels during NMDA receptor-mediated excitotoxicity may spare neurons destined to degenerate.
Accumulating evidence indicates that Mn may indirectly affect neuronal function by damaging glial cells.
The accumulation of misfolded proteins may adversely affect neuronal connectivity and plasticity and trigger cell death signalling pathways [ 2].
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