Your search for: 'author:("Hongpaisan, Jarin")' has returned 3 results. (0.007s) Save search

Authors: Hongpaisan, Jarin | Molander, Carl

Article Type: Research Article

Abstract: The distribution of stimulus evoked Fos protein-like immunoreactivity in spinal cord neurons was studied in adult rats at different survival times after sciatic nerve crush or transection and epineural repair. Fos protein-like immunoreactivity was induced either by electrical stimulation of the sciatic nerve central to the injury, at C-fiber strength, at 21, 39, and 92 days post-lesion, or by noxious heat applied to the skin of the hind paw 92 days post-lesion. The contralateral uninjured side served as control. The results with electrical stimulation showed, with some exceptions, that the distribution of c-fos expressing cells in the spinal cord on …the normal and on the previously injured side were similar after both crush and transection with repair. The main finding was an up-regulation of the number of Fos protein immunoreactive neurons in the inner portion of Rexed's lamina II. The results following heat stimulation 92 days post-lesion showed a decrease in the number of labeled neurons in most laminae after both types of injury. This was more pronounced in cases with sciatic nerve transection with repair compared to cases with crush. The results indicate time-dependent alterations in the distribution of stimulus evoked c-fos expression in spinal cord neurons during regeneration after nerve injury. Furthermore, the results from heat stimulation may indicate a slower and perhaps more incomplete restoration process after transection with repair than after crush. Show more

Keywords: Spinal cord, c-fos, Nerve regeneration, Sciatic nerve, Immediate early gene, Nerve injury

DOI: 10.3233/RNN-1993-5401

Citation: Restorative Neurology and Neuroscience, vol. 5, no. 4, pp. 249-261, 1993

Authors: Sen, Abhik | Nelson, Thomas J. | Alkon, Daniel L. | Hongpaisan, Jarin

Article Type: Research Article

Abstract: Oxidative stress and amyloid-β (Aβ) oligomers have been implicated in Alzheimer’s disease (AD). The growth and maintenance of neuronal networks are influenced by brain derived neurotrophic factor (BDNF) expression, which is promoted by protein kinase C epsilon (PKCɛ ). We investigated the reciprocal interaction among oxidative stress, Aβ, and PKCɛ levels and subsequent PKCɛ -dependent MnSOD and BDNF expression in hippocampal pyramidal neurons. Reduced levels of PKCɛ , MnSOD, and BDNF and an increased level of Aβ were also found in hippocampal neurons from autopsy-confirmed AD patients. In cultured human primary hippocampal neurons, spherical aggregation of Aβ (amylospheroids) decreased PKCɛ …and MnSOD. Treatment with t-butyl hydroperoxide (TBHP) increased superoxide, the oxidative DNA/RNA damage marker, 8-OHG, and Aβ levels, but reduced PKCɛ , MnSOD, BDNF, and cultured neuron density. These changes were reversed with the PKCɛ activators, bryostatin and DCPLA-ME. PKCɛ knockdown suppressed PKCɛ , MnSOD, and BDNF but increased Aβ. In cultured neurons, the increase in reactive oxygen species (ROS) associated with reduced PKCɛ during neurodegeneration was inhibited by the SOD mimetic MnTMPyP and the ROS scavenger NAc, indicating that strong oxidative stress suppresses PKCɛ level. Reduction of PKCɛ and MnSOD was prevented with the PKCɛ activator bryostatin in 5–6-month-old Tg2576 AD transgenic mice. In conclusion, oxidative stress and Aβ decrease PKCɛ expression. Reciprocally, a depression of PKCɛ reduces BDNF and MnSOD, resulting in oxidative stress. These changes can be prevented with the PKCɛ -specific activators. Show more

Keywords: Alzheimer’s disease, BDNF, hippocampus, MnSOD, oxidative stress, PKCɛ

DOI: 10.3233/JAD-171008

Citation: Journal of Alzheimer's Disease, vol. 63, no. 3, pp. 1173-1189, 2018

Authors: Khan, Tapan K. | Sen, Abhik | Hongpaisan, Jarin | Lim, Chol S. | Nelson, Thomas J. | Alkon, Daniel L.

Article Type: Research Article

Abstract: In Alzheimer's disease (AD) transgenic mice, activation of synaptogenic protein kinase C ε (PKCε) was found to prevent synaptotoxic amyloid-β (Aβ)-oligomer elevation, PKCε deficits, early synaptic loss, cognitive deficits, and amyloid plaque formation. In humans, to study the role of PKCε in the pathophysiology of AD and to evaluate its possible use as an early AD-biomarker, we examined PKCε and Aβ in the brains of autopsy-confirmed AD patients (n = 20) and age-matched controls (AC, n = 19), and in skin fibroblast samples from AD (n = 14), non-AD dementia patients (n = 14), and AC (n = 22). Intraneuronal …Aβ levels were measured immunohistochemically (using an Aβ-specific antibody) in hippocampal pyramidal cells of human autopsy brains. PKCε was significantly lower in the hippocampus and temporal pole areas of AD brains, whereas Aβ levels were significantly higher. The ratio of PKCε to Aβ in individual CA1 pyramidal cells was markedly lower in the autopsy AD brains versus controls. PKCε was inversely correlated with Aβ levels in controls, whereas in AD patients, PKCε showed no significant correlation with Aβ. In autopsy brains, PKCε decreased as the Braak score increased. Skin fibroblast samples from AD patients also demonstrated a deficit in PKCε compared to controls and an AD-specific change in the Aβ-oligomer effects on PKCε. Together, these data demonstrate that the relationship between Aβ levels and PKCε is markedly altered in AD patients' brains and skin fibroblasts, reflecting a loss of protective effect of PKCε against toxic Aβ accumulation. These changes of PKCε levels in human skin fibroblasts may provide an accurate, non-invasive peripheral AD biomarker. Show more

Keywords: Alzheimer's disease, amyloid-β oligomers, diagnostic assay, peripheral biomarker, PKCε

DOI: 10.3233/JAD-141221

Citation: Journal of Alzheimer's Disease, vol. 43, no. 2, pp. 491-509, 2015