Nutritional aspects importance in attention deficit hyperactivity disorder

O distúrbio de hiperatividade com déficit de atenção constitui síndrome comum na infância, pelo que é reconhecido como problema médico-social importante, sendo objeto de extensa investigação quanto aos seus determinantes, abordagens diagnosticas e formas de prevenção e tratamento. Dentro dos fatores que podem alterar a função cerebral, encontra-se a desnutrição. Os autores discutem a associação da síndrome com o estado nutricional de uma população de escolares.The attention deficit hyperactivity disorder is a common childhood syndrome that is recognized as an important medical-social problem, being the object of an exhaustive investigation related to its etiology, diagnostic approach and prevention, and treatment forms. Among the factors that can alter the cerebral function, is the malnutrition. The authors discuss the association of the syndrome with the nutritional condition of students from elementary schools

Importância dos aspectos nutricionais como fator associado à síndrome de hiperatividade com déficit de atenção Nutritional aspects importance in attention deficit hyperactivity disorder

O distúrbio de hiperatividade com déficit de atenção constitui síndrome comum na infância, pelo que é reconhecido como problema médico-social importante, sendo objeto de extensa investigação quanto aos seus determinantes, abordagens diagnosticas e formas de prevenção e tratamento. Dentro dos fatores que podem alterar a função cerebral, encontra-se a desnutrição. Os autores discutem a associação da síndrome com o estado nutricional de uma população de escolares.The attention deficit hyperactivity disorder is a common childhood syndrome that is recognized as an important medical-social problem, being the object of an exhaustive investigation related to its etiology, diagnostic approach and prevention, and treatment forms. Among the factors that can alter the cerebral function, is the malnutrition. The authors discuss the association of the syndrome with the nutritional condition of students from elementary schools

Nutritional aspects importance in attention deficit hyperactivity disorder

O distúrbio de hiperatividade com déficit de atenção constitui síndrome comum na infância, pelo que é reconhecido como problema médico-social importante, sendo objeto de extensa investigação quanto aos seus determinantes, abordagens diagnosticas e formas de prevenção e tratamento. Dentro dos fatores que podem alterar a função cerebral, encontra-se a desnutrição. Os autores discutem a associação da síndrome com o estado nutricional de uma população de escolares.The attention deficit hyperactivity disorder is a common childhood syndrome that is recognized as an important medical-social problem, being the object of an exhaustive investigation related to its etiology, diagnostic approach and prevention, and treatment forms. Among the factors that can alter the cerebral function, is the malnutrition. The authors discuss the association of the syndrome with the nutritional condition of students from elementary schools

Structural deficits in key domains of Shank2 lead to alterations in postsynaptic nanoclusters and to a neurodevelopmental disorder in humans

Postsynaptic scaffold proteins such as Shank, PSD-95, Homer and SAPAP/GKAP family members establish the postsynaptic density of glutamatergic synapses through a dense network of molecular interactions. Mutations in SHANK genes are associated with neurodevelopmental disorders including autism and intellectual disability. However, no SHANK missense mutations have been described which interfere with the key functions of Shank proteins believed to be central for synapse formation, such as GKAP binding via the PDZ domain, or Zn2+-dependent multimerization of the SAM domain. We identify two individuals with a neurodevelopmental disorder carrying de novo missense mutations in SHANK2. The p.G643R variant distorts the binding pocket for GKAP in the Shank2 PDZ domain and prevents interaction with Thr(−2) in the canonical PDZ ligand motif of GKAP. The p.L1800W variant severely delays the kinetics of Zn2+-dependent polymerization of the Shank2-SAM domain. Structural analysis shows that Trp1800 dislodges one histidine crucial for Zn2+ binding. The resulting conformational changes block the stacking of helical polymers of SAM domains into sheets through side-by-side contacts, which is a hallmark of Shank proteins, thereby disrupting the highly cooperative assembly process induced by Zn2+. Both variants reduce the postsynaptic targeting of Shank2 in primary cultured neurons and alter glutamatergic synaptic transmission. Super-resolution microscopy shows that both mutants interfere with the formation of postsynaptic nanoclusters. Our data indicate that both the PDZ- and the SAM-mediated interactions of Shank2 contribute to the compaction of postsynaptic protein complexes into nanoclusters, and that deficiencies in this process interfere with normal brain development in humans