Pictured above: Figure 3.B in the article,"The impact of tau hyperphosphorylation at Ser262 on memory and learning after global brain ischaemia in a rat model of reversible cardiac arrest." The presence of p-tau (Ser262), visualized by immunofluorescent staining which is mainly located in the processes in control group (a, b, c) and in soma and some parts of processes in the long-term recovery group of 2 min ischaemia followed by 4 weeks (d, e, f). DAPI (blue) shows nuclei staining. (S. Majd, J.H.T. Power, S.A. Koblar, H.J.M. Grantham)
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IBRO Reports is our new open access (OA) journal published by Elsevier. The sister journal to IBRO Neuroscience, it includes papers describing the results of original research on any aspect of the scientific study of the nervous system. The journal will consider for publication any article that is methodologically sound, including negative data. Replication studies are also welcomed when justified with a scientifically sound rationale.
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READ the first 8 published articles (Volume 1, December 2016) below:
(S. Majd, J.H.T. Power, S.A. Koblar, H.J.M. Grantham)
An increase in phosphorylated tau (p-tau) is associated with Alzheimer's disease (AD), and brain hypoxia. The aims of this study are to investigate the involvement of the main metabolic kinases, Liver Kinase B1 (LKB1) and Adenosine Monophosphate Kinase Protein Kinase (AMPK), in tau phosphorylation-derived memory impairment, and to study the potential contribution of the other tau kinases and phosphatases including Glycogen Synthase Kinase (GSK-3β), Protein kinase A (PKA) and Protein Phosphatase 2A (PP2A). Our data suggests a crucial role for a combined activation of tau kinases and phosphatases in adversely affecting memory and that hyperphosphorylation of tau in more than one specific site may be required to create memory deficits.
(De-Yong Liang, P. Sahbaie, Y. Sun, K.-A. Irvine, X. Shi, A. Meidahl, P. Liu, T.-Z. Guo, D.C. Yeomans, J.D. Clark)
Chronic pain after traumatic brain injury (TBI) is very common, but the mechanisms linking TBI to pain and the pain-related interactions of TBI with peripheral injuries are poorly understood. In these studies we pursued the hypothesis that TBI pain sensitization is associated with histone acetylation in the rat lateral fluid percussion model. Findings demonstrate that TBI induces sustained nociceptive sensitization, and changes in spinal neuronal histone proteins may play an important role.
(E. Ruchti, P.J. Roach, A.A. DePaoli-Roach, P.J. Magistretti, I. Allaman)
To achieve further insight into the role of PTG in the regulation of astrocytic glycogen, its levels of expression were manipulated in primary cultures of mouse cortical astrocytes using adenovirus-mediated overexpression of tagged-PTG or siRNA to downregulate its expression. Resulting observations point to a major role of PTG in the regulation of glycogen synthesis in astrocytes and indicate that conditions leading to changes in PTG expression will directly impact glycogen levels in this cell type.
(M.L. Slaker, J.H. Harkness, B.A. Sorg)
A clearly-defined and unified method for assessing the intensity of perineuronal nets (PNNs) is critical to allow us to make comparisons across studies and to advance our understanding of how PNN plasticity contributes to normal brain function and brain disease states. Here we examined methods of PNN intensity quantification and demonstrate that creating a region of interest around each PNN and subtracting appropriate background is a viable method for PNN intensity quantification that can be automated
(R.S. Chaves, A.I. Kazi, C.M. Silva, M.F. Almeida, R.S. Lima, D.C. Carrettiero, M. Demasi, M.F.R. Ferrari)
To better understand the biological role of the protein aggregation with regard its effects in cellular homeostasis, the present study investigated the role of insoluble Tau and Tau aggregates on crucial cellular parameters such as redox homeostasis, proteasome activity and autophagy in hippocampal cell cultures and hippocampus of aged Lewis rats using a rotenone-induced aggregation model. Our experimental design allowed us to demonstrate that rotenone exposure induces Tau hyperphosphorylation and aggregation in a concentration and time-dependent manner.
(M.F. Almeida, R.S. Chaves, C.M. Silva, J.C.S. Chaves, K.P. Melo, M.F.R. Ferrari)
Physical exercise can attenuate the effects of aging on the central nervous system by increasing the expression of neurotrophins such as brain-derived neurotrophic factor (BDNF), which promotes dendritic branching and enhances synaptic machinery, through interaction with its receptor TrkB. In the present study, it was found that early neurodegeneration is accompanied by decrease in BDNF signaling, in the absence of hyperphosphorylated tau aggregation, in hippocampus of 11 months old Lewis rats exposed to rotenone. It was also demonstrated that moderate physical activity prevents the impairment of BDNF system in aged rats, which may contribute to delay neurodegeneration.
(I.M. Fuentes, N.K. Walker, A.N. Pierce, B.R. Holt, E.R. Di Silvestro, J.A. Christianson)
In this study, researchers investigated whether neonatal maternal separation (NMS) would increase susceptibility to experimental colitis or exposure to acute or chronic stress. Results suggest that NMS in mice disrupts inflammatory- and stress-induced gene expression in the colon, potentially contributing towards an exaggerated response to specific stressors later in life.
(E. Hanssona, T. Wernera, U. Björklunda, E. Skiöldebrandb)
This study aimed to test pharmaceutical compounds targeting astrocytes showing inflammatory dysregulation. Other aims of the study were to prevent astrocytes from becoming inflammatory-reactive and to restore inflammatory dysregulated cellular changes. Results indicated that the study's drug combination prevented the LPS- and tryptase-induced inflammatory dysregulation, and it could also restore the LPS- and tryptase-treated cells back to a normal physiological level in terms of the analyzed parameters.