Your doctor should be excited about reading these types of research. If not, why the hell are you seeing them? They are supposed to know more than you.
http://europepmc.org/abstract/MED/23988450
Biomolecular
Dynamics Laboratory, Department of Biomolecular Networks, Graduate
School of Frontier Biosciences. Electronic address:
fujiwara@anat3.med.osaka-u.ac.jp.
Neurodegeneration
causes dysfunction and degeneration of neurons and is triggered by
various factors including genetic defects, free radicals, injury, and
glutamate excitotoxicity.
Among those, glutamate excitotoxicity is implicated in chronic disorders including AD and ALS, and in acute insults in the CNS including traumatic brain injury.
Neurological disorders show hallmark morphological abnormalities such as
axon degeneration and
cell body death.
The molecular mechanisms underlying excitotoxicity-induced
neurodegeneration are complex and deciphering a molecular mechanism from
one angle is beneficial to understand the process, however, still
difficult to develop strategies to suppress excitotoxicity-induced
degeneration due to existence of other mechanisms.
Thus, directly identifying compounds that can modulate
excitotoxicity-induced neurodegeneration and subsequently clarifiying
the molecular mechanism is a valid approach to develop effective
strategies to suppress neurodegeneration.
We searched for compounds that can suppress excitotoxicity-induced
neurodegeneration and found that CP-31398, a known compound that can
rescue the structure and function of the
tumor suppressor protein
p53 mutant form and stabilize the active conformation of the
p53 wild-type form, suppresses excitotoxicity-induced
axon degeneration and
cell body death.
Moreover, CP-31398 suppresses mitochondrial dysfunction which has a strong correlation with excitotoxicity.
Thus, our findings identify a compound that can serve as a novel modulator of neurodegeneration induced by
glutamate excitotoxicity.
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