Chapters authored
Animal Model of Parkinson Disease: Neuroinflammation and Apoptosis in the 6-Hydroxydopamine-Induced Model
6-Hydroxydopamine (6-OHDA), a synthetic neurotoxin, has been used to generate animal models of Parkinson’s disease (PD). Even though 6-OHDA induced neurodegenerative model in rat, it does not reproduce all the symptoms of the disease, but it does replicate most of the cellular processes such as oxidative stress, neurodegeneration, neuroinflammation and apoptotic neuronal death. The knowledge of the mechanisms involved in neurodegeneration is relevant to define possible therapeutic targets for PD.
Part of the book: Experimental Animal Models of Human Diseases
Stress and Cognition: Psychological Basis and Support Resources
Executive functions are processes that help in tasks such as reasoning, planning, troubleshooting, and management of the individual’s own life. A consequence of the specific connections of stress is that executive functions tend to be interrupted when the stimulation load is so big that the individual becomes stressed. The level of cellular stress becomes evident with the increase of cortisol. Cellular processes such as inflammation, proliferation/death, and oxidative stress have been shown in murine models resembling cognitive impairment in humans. This impairment translates into behavioral changes, loss of memory, inability for decision-making, and attention problems. The incorporation of factors, such as drug use and bullying, promotes the impairment of executive functions. Resorting to strategies, such as exercising, environmental enrichment, and changes in the diet, constitutes an excellent aid in the promotion of academic achievement. In this chapter, we discuss the impact of stress on cognitive executive functions associated with academic achievement and also suggest strategies to reduce the impact of stressing factors.
Part of the book: Health and Academic Achievement
The Causative and Curative Roles of Brain-Derived Neurotrophic Factor in Parkinson’s Disease
Parkinson’s disease (PD) is characterized by the activation of degenerative and inflammatory processes in brain circuits that control movement and, according to the degree of progression of the damage, can cause neuropsychological disorders such as cognitive dysfunction. Changes in gene expression profile or post-translational modifications in secretory proteins such as neurotrophic factors could define the disease progression. Brain-derived neurotrophic factor (BDNF) is relevant, because it not only participates in neuronal survival, neurotransmission, dendritic growth and cellular communication but also in disease progression. In this chapter, considering both experimental evidences and clinical reports, the authors will analyze the contribution of BDNF as one of the causes of neurodegeneration and neuroinflammation; discuss the participation of this neurotrophic factor in the development of cognitive dysfunction, and finally the scope of novel BDNF-based therapies for PD.
Part of the book: Parkinson's Disease and Beyond