ABSTRACT
Rheumatic fever (RF) and rheumatic heart disease (RHD) follow untreated S. pyogenes throat infections in children who present susceptible genes that favor the development of autoimmune reactions. In this review, we focus on the genes that confer susceptibility and on the autoimmune reactions that occur due to molecular mimicry between human-tissue proteins and streptococcal M protein. Polyarthritis is the initial manifestation, which can evolve to carditis and severe valve damage; these culminate in rheumatic heart disease (RHD) or Sydenham's chorea, which affects the central nervous system. A perspective on vaccine development to prevent the disease is also discussed.
Subject(s)
Rheumatic Heart Disease/metabolism , Rheumatic Heart Disease/prevention & control , Vaccines/therapeutic use , Autoimmunity , Chorea/etiology , Chorea/immunology , Chorea/metabolism , Chorea/prevention & control , Cytokines/metabolism , Histocompatibility Antigens Class II/genetics , Humans , Molecular Mimicry , Rheumatic Fever/etiology , Rheumatic Fever/immunology , Rheumatic Fever/metabolism , Rheumatic Fever/prevention & control , Rheumatic Heart Disease/etiology , Rheumatic Heart Disease/immunology , Streptococcus pyogenesABSTRACT
Brain-derived neurotrophic factor (BDNF) is the most widely distributed neurotrophin in the CNS, where it plays several pivotal roles in synaptic plasticity and neuronal survival. As a consequence, BDNF has become a key target in the physiopathology of several neurological and psychiatric diseases. Recent studies have consistently reported altered levels of BDNF in the circulation (i.e., serum or plasma) of patients with major depression, bipolar disorder, Alzheimer's disease, Huntington's disease and Parkinson's disease. Correlations between serum BDNF levels and affective, cognitive and motor symptoms have also been described. BDNF appears to be an unspecific biomarker of neuropsychiatric disorders characterized by neurodegenerative changes.