However, TDP-43 has since been detected in conditions such as Alzheimer’s disease (AD) and dementia with Lewy bodies (DLB) but is often confined to the limbic region rather than the more widespread pattern seen in FTLD-TDP. Previous work has suggested some relationship between hippocampal sclerosis and TDP-43 expression. A number of AD cases of both moderate and high stage were examined Trichostatin A mw to determine whether the pattern of TDP-43

immunohistochemical expression differed and whether any relationship to hippocampal sclerosis could be detected. Cases of hippocampal sclerosis from surgical epilepsy specimens were examined to determine whether hippocampal sclerosis alone could cause abnormal TDP-43 expression. To establish whether abnormal TDP-43 expression in other neurodegenerative diseases resembled the pattern and distribution in FTLD-TDP we examined multiple blocks from a variety of neurodegenerative conditions. In 75% of cases of high-stage AD there was abnormal TDP-43 positivity compared to 57% of moderate-stage AD. While the abnormal TDP-43 positivity was confined to the limbic regions in the moderate stages, occasional cases in the high stages showed neocortical positivity. Also amygdala and/or entorhinal positivity appeared to precede positivity in the dentate gyrus. No relationship could be established between abnormal TDP-43

expression and degree of hippocampal sclerosis either in the surgical or autopsy cases. The pattern of distribution of TDP-43 inclusions from cases of dementia pugilistica most closely resembled that in FTLD-TDP. This raises the question as to whether there may be some shared pathogenic https://www.selleckchem.com/products/Vincristine-Sulfate.html mechanisms between the two conditions. “
“F. Junyent, L. de Lemos, E. Verdaguer, M. Pallàs, J. Folch, C. Beas-Zárate, A. Camins and C. Auladell (2012) Neuropathology and Applied Neurobiology38, 311–321 Lack of Jun-N-terminal kinase 3 (JNK3) does not protect

against neurodegeneration induced by 3-nitropropionic acid Aims: 3-Nitropropionic acid (3-NP) is a toxin that replicates most of the clinical and pathophysiological symptoms of Huntington’s disease, Thalidomide inducing neurodegeneration in the striatum due to the inhibition of mitochondrial succinate dehydrogenase. Different pathways have been implicated in the cell death induced by 3-NP in rodents. One of them is the Jun-N-terminal kinase (JNK) pathway, which may play a role in the neurodegenerative process in different diseases. Moreover, the lack of one isoform of JNK (JNK3) has been associated with neuroprotection in different experimental models of neurodegeneration. Therefore, in the present study the role of JNK3 in the experimental Huntington’s model induced by 3-NP administration was evaluated. Methods: 3-NP was intraperitoneally administered once a day for 3 days to wild-type and Jnk3-null mice. Coronal brain sections were used to determine cell death and astrogliosis in striatum.