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Reactive oxygen species (ROS) play an important role in a rat model of neuropathic pain

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Long-Term Dietary Strawberry, Spinach, or Vitamin E Supplementation Retards the Onset of Age-Related Neuronal Signal-Transduction and Cognitive Behavioral Deficits

Phytochemicals present in antioxidant-rich foods such as spinach may be beneficial in retarding functional age-related CNS and cognitive behavioral deficits and, perhaps, may have some benefit in neurodegenerative disease.
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NFκB-Activated Astroglial Release of Complement C3 Compromises Neuronal Morphology and Function Associated with Alzheimer’s Disease

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A Role for Calcineurin in Alzheimer’s Disease

This review details the evidence of CaN hyperactivity in ‘normal’ aging, models of AD, and actual disease pathogenesis; elaborates on how this could manifest as memory impairment, neuroinflammation, hyperphosphorylated tau, and neuronal death.
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Intermediate- and long-term recognition memory deficits in Tg2576 mice are reversed with acute calcineurin inhibition

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Acetyl-L-carnitine enhances the response of PC12 cells to nerve growth factor.

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Expression of nerve growth factor in the dorsal root ganglion after peripheral nerve injury

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Amyloid‐β oligomers impair fear conditioned memory in a calcineurin‐dependent fashion in mice

Mice given a single intracerebroventricular injection of Aβ oligomers exhibited increased CaN activity and decreased pCREB, a transcription factor involved in proper synaptic function, accompanied by decreased memory in a fear conditioning task, which indicates that CaN activation may play a central role in mediating synaptic and memory disruption induced by acute oligomeric Aβ treatment in mice.
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Acute inhibition of calcineurin restores associative learning and memory in Tg2576 APP transgenic mice

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Selective induction of calcineurin activity and signaling by oligomeric amyloid beta

It is found that young Tg2576 transgenic mice, which accumulate Aβ and develop cognitive impairments prior to plaque deposition, have high central nervous system activity of calcineurin (CaN), a phosphatase involved in negative regulation of memory function via inactivation of the transcription factor cAMP responsive element binding proteins (CREB), and display CaN‐dependent memory deficits, suggesting a role for CaN in mediating effects of oligomeric Aβ on neural cells.
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