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Alterations in Trk A, Trk B and Trk C Receptor Immunoreactivities in Parietal Cortex and Cerebellum in Alzheimer’s Disease
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The neurotrophins nerve growth factor, brain-derived neurotrophic factor and neurotrophin-3 bind to the tyrosine kinase (trk) receptors trk A, trk B and trk C, respectively, with high affinity. We investigated the expression of the trk receptors in the parietal cortex (PC) and cerebellum of patients with Alzheimer’s disease (AD) and age-matched controls. Cortical layers II–VI displayed a distinct cellular immunoreactivity for trk A and C with an emphasis in the pyramidal neurons of layers III and V. Trk B immunoreactivity was primarily located in the deeper cortical layers with a predominance in layer V. There was a decrease in trk A and C immunoreactivity in the PC of AD cases, while trk B density appeared to be unchanged. In addition, cerebellar Purkinje cells revealed a distinct immunoreactivity for trk C both in control and AD cases, suggesting trk C may be important in the maintenance of these cells in the aged brain.
Title: Alterations in Trk A, Trk B and Trk C Receptor Immunoreactivities in Parietal Cortex and Cerebellum in Alzheimer’s Disease
Description:
The neurotrophins nerve growth factor, brain-derived neurotrophic factor and neurotrophin-3 bind to the tyrosine kinase (trk) receptors trk A, trk B and trk C, respectively, with high affinity.
We investigated the expression of the trk receptors in the parietal cortex (PC) and cerebellum of patients with Alzheimer’s disease (AD) and age-matched controls.
Cortical layers II–VI displayed a distinct cellular immunoreactivity for trk A and C with an emphasis in the pyramidal neurons of layers III and V.
Trk B immunoreactivity was primarily located in the deeper cortical layers with a predominance in layer V.
There was a decrease in trk A and C immunoreactivity in the PC of AD cases, while trk B density appeared to be unchanged.
In addition, cerebellar Purkinje cells revealed a distinct immunoreactivity for trk C both in control and AD cases, suggesting trk C may be important in the maintenance of these cells in the aged brain.
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