Abstract
Parkinson’s disease (PD) is a neurodegenerative disease characterized by the loss of midbrain dopamine (mDA) neurons. Clinical trials using human embryonic midbrain tissue for transplantation have provided proof of concept that cell replacement therapy (CRT) can lead to not only symptomatic relief, but also changes in the course of disease and withdrawal of medication. Human pluripotent stem cells are currently regarded as the main candidate cell type for CRT because they are readily available, expandable, and can be standardized and differentiated into mDA neurons capable of inducing functional recovery in animal models of PD. However, protocols for mDA differentiation are still far from optimal and require further improvement. We previously found that members of the Wnt family of morphogens regulate multiple aspects of mDA neuron development [1]. Different branches of the Wnt signaling pathway, such as Wnt/β-catenin, activated by Wnt1, and Wnt/PCP, activated by Wnt5a, have been thought to regulate separate or opposing functions. However, we found that Wnt5a cooperates with Wnt1 to promote mDA neurogenesis and that Wnt1 cooperates with Wnt5a to promote the differentiation of postmitotic mDA neuroblasts [2]. We are currently applying this knowledge to improve protocols for the differentiation of human stem cells into mDA neurons suitable for transplantation and functional recovery in animal models for PD [3].
Highlights
Alzheimer’s disease (AD) is an incurable neurodegenerative disease characterized by progressive dementia
The results of the present study indicate that development of the neuronal hypoxic tolerance induced by the three-trial, in contrast to one-trial, mild hypoxic preconditioning is apparently largely associated with the activation of CREB, as well as brain-derived neurotrophic factor (BDNF) and Bcl-2 overexpression
No significant differences in serum level of Solubile form of RAGE (sRAGE) where found between rapidly progressing and slow progressing subgroup of multiple sclerosis (MS) patients.Our results suggest for the role of sRAGE in MS ethiopathogenesis, but we did not find any association of sRAGE in serum with the rate of MS disability progression
Summary
Alzheimer’s disease (AD) is an incurable neurodegenerative disease characterized by progressive dementia. The aim of the study was to characterize the effects of streptozocin (STZ)-indced diabetes on learning and memory of 5XFAD and wild-type (WT) mice in Morris water maze (MWM) at ages 2 and 6 months and on brain amyloid load. Existing evidence suggests GABAergic system is involved in pathophysiology of Alzheimer’s disease (AD) via inhibitory interneuron deficits (Verret et al, 2012) and decrease in functional GABAA receptors (Limon et al, 2012). Our concept: low doses of muscimol may prevent learning/memory deficits in intracerebroventricular (icv) streptozocin (STZ)-induced AD nontransgenic rat model. The Sigma-1 receptor is a chaperone protein that modulates intracellular calcium signalling of the endoplasmatic reticulum and is involved in learning and memory processes.The aim of the present study was to compare in vitro Ca2+ concentration modulating activity and in vivo behavioural effects of enantiomers of methylphenylpiracetam, a novel positive allosteric modulator of Sigma-1 receptors
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