Profound and selective loss of catalytic TrkB immunoreactivity in Alzheimer's disease
SJ Allen, GK Wilcock, D Dawbarn - Biochemical and biophysical research …, 1999 - Elsevier
SJ Allen, GK Wilcock, D Dawbarn
Biochemical and biophysical research communications, 1999•ElsevierBrain-derived neurotrophic factor (BDNF) is known to have trophic effects on various
neurons, throughout the brain and spinal cord, via its high-affinity tyrosine kinase receptor
TrkB. It has been reported that the mRNA for this neurotrophin is reduced in Alzheimer's
disease (AD) brain. We have examined, by Western blotting, the catalytic (p145) and
noncatalytic or truncated (p95) forms of TrkB and find that, in both the temporal and frontal
cortex, there is a selective loss of immunoreactive-positive staining for the catalytic or kinase …
neurons, throughout the brain and spinal cord, via its high-affinity tyrosine kinase receptor
TrkB. It has been reported that the mRNA for this neurotrophin is reduced in Alzheimer's
disease (AD) brain. We have examined, by Western blotting, the catalytic (p145) and
noncatalytic or truncated (p95) forms of TrkB and find that, in both the temporal and frontal
cortex, there is a selective loss of immunoreactive-positive staining for the catalytic or kinase …
Brain-derived neurotrophic factor (BDNF) is known to have trophic effects on various neurons, throughout the brain and spinal cord, via its high-affinity tyrosine kinase receptor TrkB. It has been reported that the mRNA for this neurotrophin is reduced in Alzheimer's disease (AD) brain. We have examined, by Western blotting, the catalytic (p145) and noncatalytic or truncated (p95) forms of TrkB and find that, in both the temporal and frontal cortex, there is a selective loss of immunoreactive-positive staining for the catalytic or kinase form compared with the truncated form. This may have important consequences for the neurotrophic support of vulnerable neurons in AD.
Elsevier
