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Severe increases in these toxic species are deleterious to dopaminergic neurons and may induce neuronal degeneration.
Hyperglycemia increases the NMDA receptor-mediated calcium entry into the neurons and may induce neuronal excitotoxicity through an activation cascade ending by the release of ROS.
Human immunodeficiency virus type I (HIV-1 -specific HIV-1 -specificduce neuronal apoptosis, but tHIV-1 -specificduction of HIV-1 gproteinsuced, direct neuronal apoptosis remayns unclear.
In turn, increased extracellular β-amyloid peptide production may induce neuronal apoptosis, leading to further deposition of senile plaques.
These findings suggest that soluble Aβ1-42 may induce neuronal hyperexcitation by increasing the amplitude of INaP and that RLZ can inhibit the Aβ1-42-induced abnormal neuronal activity.
However, glucocorticoid supplementation leads to elevated serum glucose levels and may induce neuronal damage [ 100].
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This event results in drastic reduction of the bioactivity of NGF for the cholinergic neurons and may further induce neuronal cell death (Bruno et al., 2009).
Therefore, hypoxic ischemic injuries may specifically induce neuronal death in these areas.
In this paradigm, impaired mitochondrial dynamics and clearance result in the accumulation of damaged and dysfunctional mitochondria, which may directly induce neuronal dysfunction and death.
The low occurrence and significant delay of apoptosis among cortical neurons lacking presenilins suggest that loss of presenilins may induce apoptotic neuronal death through disruption of cellular homeostasis rather than direct activation of apoptosis pathways.
Recent studies increasingly indicated that soluble, pre-fibrillar Aβ assemblies rather than mature fibrils may induce early neuronal alterations, leading to physiological interruption before cell death is detectable [47].
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