RESUMO
Chronic traumatic encephalopathy (CTE) is caused by progressive neurodegeneration associated with repetitive head impacts. This disease is more common in professionals who practice contact sports, resulting in a concussion and subconcussive trauma. CTE is characterized by the accumulation of hyperphosphorylated tau protein in neurons, astrocytes, and frontotemporal lobe degeneration. Symptoms are usually nonspecific and overlap with other neurodegenerative diseases, such as Alzheimer's disease and frontotemporal dementia, making it difficult to provide drug treatment for patients with this comorbidity. Therefore, the objective of this article is to present an updated review of the pharmacological treatment of chronic traumatic encephalopathy and its challenges.
Assuntos
Doença de Alzheimer , Concussão Encefálica , Encefalopatia Traumática Crônica , Demência Frontotemporal , Humanos , Encefalopatia Traumática Crônica/diagnóstico , Encefalopatia Traumática Crônica/tratamento farmacológico , Encefalopatia Traumática Crônica/etiologia , Concussão Encefálica/complicações , Concussão Encefálica/tratamento farmacológico , Doença de Alzheimer/complicações , Proteínas tau , AstrócitosRESUMO
Over the past 70 years, the understanding of Autism Spectrum Disorder (ASD) improved greatly and is characterized as a heterogeneous neuropsychiatric syndrome. ASD is characterized by difficulties in social communication, restricted and repetitive behavior, interests, or activities. And it is often described as a combination of genetic predisposition and environmental factors. There are many treatments and approaches to ASD, including pharmacological therapies with antipsychotics, antidepressants, mood regulators, stimulants, and behavioral ones. However, no treatment is capable of reverting ASD. This review provides an overview of animal models of autism. We summarized genetic and environmental models and then valproic acid treatment as a useful model for ASD. As well as the main therapies and approaches used in the treatment, relating them to the neurochemical pathways altered in ASD, emphasizing the pharmacological potential of peptides and bioinspired compounds found in animal venoms as a possible future treatment for ASD.