Novel pro-neurogenic compound that lowers synaptic Aβgeneration shows cognitive benefit and reduced hippocampal levels of insoluble and oligomeric Aβin vivo in an Alzheimer’s mouse model Sam Gandy, M.D., Ph.D. ount Sinai Chair in Alzheimer’s Disease Researc Mount Sinai School of Medicine and James J Peters VA Medical Center in collaboration with BrainCells, Inc. Alzheimer’s Disease International March 8, 2012
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Novel pro-neurogenic compound that lowers synaptic A β generation shows cognitive benefit and reduced hippocampal levels of insoluble and oligomeric.
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Novel pro-neurogenic compound that lowers synaptic
Aβ generation shows cognitive benefit and reduced hippocampal levels of insoluble and
oligomeric Aβ in vivo in an Alzheimer’s mouse model
Sam Gandy, M.D., Ph.D.Mount Sinai Chair in Alzheimer’s Disease Research
Mount Sinai School of Medicine andJames J Peters VA Medical Center
in collaboration withBrainCells, Inc.
Alzheimer’s Disease InternationalMarch 8, 2012
Baseline 78 wks Bapineuzumab Rx
Might there be a safe and novel intervention that
arrests progression of amyloidosis, enhances cognitive function, and
stimulates hippocampal repair (neurogenesis)?
Synaptic accumulation of Aβ42 is proposed to bea major mechanism in cause/progression of AD:
Is metabotropic (mGluR) signaling involved in regulating Aβ42 metabolism at the synapse?
“Synaptosome” or “synaptoneurosome”
DCG-IV stimulatesgeneration of Aβ42
but not Aβ40
Pretreatment with mGluR2/3 antagonist
blocks DCG-IV stimulatedgeneration of Aβ42
Might there be a safe and novel intervention that
arrests progression of amyloidosis, enhances cognitive function, and
stimulates hippocampal repair (neurogenesis)?
mGluR2/3 antagonist BCI-838 (632) reduces levels of
various Aβconformers in hippocampus and cortex
Might there be a safe and novel intervention that
arrests progression of amyloidosis, enhances cognitive function, and
that may constitute a novel approach to early stages of Alzheimer’s disease that combines arrest of progression of amyloid pathology with stimulation of cognitive function and hippocampal repair (neurogenesis).