  In recent years, many molecular and environmental factors have been studied
to understand how synaptic plasticity is modulated. Sleep, as an evolutionary
conserved biological function, has shown to be a critical player for the
consolidation and filtering of synaptic circuitry underlying memory traces.
Although sleep disturbances do not alter normal memory consolidation, they may
reflect fundamental circuit malfunctions that can play a significant role in
exacerbating diseases, such as autism and Alzheimer's disease. Very recently,
scientists sought to answer part of this enigma and they identified p75
neurotrophic receptor (p75NTR) as a critical player in mediating impairments in
hippocampal-dependent associative plasticity upon sleep deprivation. This paper
will review the role of the p75NTR, critically discuss the impact and
implications of this research as the bridge for sleep research and neurological
diseases.
