Profound and selective loss of catalytic TrkB immunoreactivity in Alzheimer's disease
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作者:
Allen, SJ
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Univ Bristol, Bristol Royal Infirm, Dept Med Care Elderly, Mol Neurobiol Unit, Bristol BS2 8HW, Avon, EnglandUniv Bristol, Bristol Royal Infirm, Dept Med Care Elderly, Mol Neurobiol Unit, Bristol BS2 8HW, Avon, England
Allen, SJ
[1
]
Wilcock, GK
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机构:Univ Bristol, Bristol Royal Infirm, Dept Med Care Elderly, Mol Neurobiol Unit, Bristol BS2 8HW, Avon, England
Wilcock, GK
Dawbarn, D
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机构:Univ Bristol, Bristol Royal Infirm, Dept Med Care Elderly, Mol Neurobiol Unit, Bristol BS2 8HW, Avon, England
Dawbarn, D
机构:
[1] Univ Bristol, Bristol Royal Infirm, Dept Med Care Elderly, Mol Neurobiol Unit, Bristol BS2 8HW, Avon, England
[2] Frenchay Hosp, Dept Care Elderly, Bristol BS16 1LE, Avon, England
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. (C) 1999 Academic Press.