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Background: Diet and physical activity are important factors in the prevention of childhood overweight. This article stresses the importance of effective communication for health behavior. Methods: Transcription, description and analysis of standardized focus group discussions (FGD) in seven European countries using standardized questioning routes. Results: Parents are well informed about health-related topics for children, but seem to have difficulties understanding their role in promoting healthy behavior. They mentioned health-related rules, but our results show limited communication between parents and children, and no follow-up of rules. Consequently, children do not understand rules about good health and do not follow them. Conclusion: Effective and sustainable intervention programs should focus on educational methods and, using parental role modeling, facilitate parents' comprehension of their key role in setting rules and controlling them in order to communicate good health behavior to their children.

Background: The current study aimed at describing influencing factors for physical activity among young children to determine the best approaches for developing the IDEFICS community based intervention. Methods: In 8 European sites a trained moderator conducted a minimum of 4 focus groups using standardized questioning guides. A total of 56 focus groups were conducted including 36 focus groups with parents and 20 focus groups with children, of which 74 were boys and 81 girls. Key findings were identified through independent reviews of focus group summary reports using content analysis methods. Findings: Findings were generally consistent across countries. The greatest emphasis was on environmental physical (eg, seasonal influences, availability of facilities and safety), institutional (eg, length of breaks at school), and social factors (eg, role modeling of parents). Most cited personal factors by parents were age, social economical status, and perceived barriers. Both children and parents mentioned the importance of children's preferences. Conclusions: To increase physical activity levels of young children the intervention should aim at creating an environment (physical, institutional, social) supportive of physical activity. On the other hand strategies should take into account personal factors like age and social economical status and should consider personal barriers too., Group Author(s): IDEFICS Consortium

BACKGROUND: The current study aimed at describing influencing factors for physical activity among young children to determine the best approaches for developing the IDEFICS community based intervention. METHODS: In 8 European sites a trained moderator conducted a minimum of 4 focus groups using standardized questioning guides. A total of 56 focus groups were conducted including 36 focus groups with parents and 20 focus groups with children, of which 74 were boys and 81 girls. Key findings were identified through independent reviews of focus group summary reports using content analysis methods. FINDINGS: Findings were generally consistent across countries. The greatest emphasis was on environmental physical (eg, seasonal influences, availability of facilities and safety), institutional (eg, length of breaks at school), and social factors (eg, role modeling of parents). Most cited personal factors by parents were age, social economical status, and perceived barriers. Both children and parents mentioned the importance of children's preferences. CONCLUSIONS: To increase physical activity levels of young children the intervention should aim at creating an environment (physical, institutional, social) supportive of physical activity. On the other hand strategies should take into account personal factors like age and social economical status and should consider personal barriers too. © 2010 Human Kinetics, Inc., IDEFICS (EU-project)

Neuronal degeneration is a commanding event in Alzheimer's disease (AD). Neuronal loss is one of the major hallmarks and is frequently reported in regions with presence of neuritic plaques (NPs) and neurofibrillary tangles (NFTs) The causative role of â-amyloid (Aâ) and tau protein in neurofibrillary pathology is controversial, and the main trigger for neurodegeneration in AD is still unknown. Thus we investigated neuronal and glial changes in the principal inferior olivary nucleus (PO) in normal aging and AD. This region is known not to develop NPs or NFTs in sporadic AD, although a few diffuse Aâ accumulations can be found. To obtain a precise number of cells an unbiased quantitative methodology should be applied. In the first study using a stereological method, optical fractionator, we estimated the total number of neurons in PO, where we reported a significant neuronal loss of up to 34% in AD group compared to age-matched controls. It is well established that neurons are in very close contact and cohabitation with glial cells. Whether neurons in PO die solely or other cells are involved was not known. In the second study we expanded a quantitative analysis and estimated a total number of oligodendrocytes and astrocytes in PO in AD and control brains. The total number of astrocytes remained unchanged, but oligodendroglial cell number was diminished by 46% indicating interdependent degeneration among neurons and oligodendrocytes. We could conclude that neurodegeneration takes place in AD brains, even in absence of neurofibrillary pathology. The patomechanisms sins behind the neuronal loss are still unknown. In the third study we applied immunohistochemistry with unbiased quantification and ELISA method to analyse astroglial markers (S100B, GFAP and vimentin) known to be involved in neurodegeneration. A 2-fold significant increase of S100B was found by immunohistochemistry and by ELISA in AD vs. age-matched controls. Due to the fact that S100B can have both benefic

Neuronal degeneration is a commanding event in Alzheimer's disease (AD). Neuronal loss is one of the major hallmarks and is frequently reported in regions with presence of neuritic plaques (NPs) and neurofibrillary tangles (NFTs) The causative role of â-amyloid (Aâ) and tau protein in neurofibrillary pathology is controversial, and the main trigger for neurodegeneration in AD is still unknown. Thus we investigated neuronal and glial changes in the principal inferior olivary nucleus (PO) in normal aging and AD. This region is known not to develop NPs or NFTs in sporadic AD, although a few diffuse Aâ accumulations can be found. To obtain a precise number of cells an unbiased quantitative methodology should be applied. In the first study using a stereological method, optical fractionator, we estimated the total number of neurons in PO, where we reported a significant neuronal loss of up to 34% in AD group compared to age-matched controls. It is well established that neurons are in very close contact and cohabitation with glial cells. Whether neurons in PO die solely or other cells are involved was not known. In the second study we expanded a quantitative analysis and estimated a total number of oligodendrocytes and astrocytes in PO in AD and control brains. The total number of astrocytes remained unchanged, but oligodendroglial cell number was diminished by 46% indicating interdependent degeneration among neurons and oligodendrocytes. We could conclude that neurodegeneration takes place in AD brains, even in absence of neurofibrillary pathology. The patomechanisms sins behind the neuronal loss are still unknown. In the third study we applied immunohistochemistry with unbiased quantification and ELISA method to analyse astroglial markers (S100B, GFAP and vimentin) known to be involved in neurodegeneration. A 2-fold significant increase of S100B was found by immunohistochemistry and by ELISA in AD vs. age-matched controls. Due to the fact that S100B can have both benefic

Neuronal degeneration is a commanding event in Alzheimer's disease (AD). Neuronal loss is one of the major hallmarks and is frequently reported in regions with presence of neuritic plaques (NPs) and neurofibrillary tangles (NFTs) The causative role of â-amyloid (Aâ) and tau protein in neurofibrillary pathology is controversial, and the main trigger for neurodegeneration in AD is still unknown. Thus we investigated neuronal and glial changes in the principal inferior olivary nucleus (PO) in normal aging and AD. This region is known not to develop NPs or NFTs in sporadic AD, although a few diffuse Aâ accumulations can be found. To obtain a precise number of cells an unbiased quantitative methodology should be applied. In the first study using a stereological method, optical fractionator, we estimated the total number of neurons in PO, where we reported a significant neuronal loss of up to 34% in AD group compared to age-matched controls. It is well established that neurons are in very close contact and cohabitation with glial cells. Whether neurons in PO die solely or other cells are involved was not known. In the second study we expanded a quantitative analysis and estimated a total number of oligodendrocytes and astrocytes in PO in AD and control brains. The total number of astrocytes remained unchanged, but oligodendroglial cell number was diminished by 46% indicating interdependent degeneration among neurons and oligodendrocytes. We could conclude that neurodegeneration takes place in AD brains, even in absence of neurofibrillary pathology. The patomechanisms sins behind the neuronal loss are still unknown. In the third study we applied immunohistochemistry with unbiased quantification and ELISA method to analyse astroglial markers (S100B, GFAP and vimentin) known to be involved in neurodegeneration. A 2-fold significant increase of S100B was found by immunohistochemistry and by ELISA in AD vs. age-matched controls. Due to the fact that S100B can have both benefic

Neuronal degeneration is a commanding event in Alzheimer's disease (AD). Neuronal loss is one of the major hallmarks and is frequently reported in regions with presence of neuritic plaques (NPs) and neurofibrillary tangles (NFTs) The causative role of â-amyloid (Aâ) and tau protein in neurofibrillary pathology is controversial, and the main trigger for neurodegeneration in AD is still unknown. Thus we investigated neuronal and glial changes in the principal inferior olivary nucleus (PO) in normal aging and AD. This region is known not to develop NPs or NFTs in sporadic AD, although a few diffuse Aâ accumulations can be found. To obtain a precise number of cells an unbiased quantitative methodology should be applied. In the first study using a stereological method, optical fractionator, we estimated the total number of neurons in PO, where we reported a significant neuronal loss of up to 34% in AD group compared to age-matched controls. It is well established that neurons are in very close contact and cohabitation with glial cells. Whether neurons in PO die solely or other cells are involved was not known. In the second study we expanded a quantitative analysis and estimated a total number of oligodendrocytes and astrocytes in PO in AD and control brains. The total number of astrocytes remained unchanged, but oligodendroglial cell number was diminished by 46% indicating interdependent degeneration among neurons and oligodendrocytes. We could conclude that neurodegeneration takes place in AD brains, even in absence of neurofibrillary pathology. The patomechanisms sins behind the neuronal loss are still unknown. In the third study we applied immunohistochemistry with unbiased quantification and ELISA method to analyse astroglial markers (S100B, GFAP and vimentin) known to be involved in neurodegeneration. A 2-fold significant increase of S100B was found by immunohistochemistry and by ELISA in AD vs. age-matched controls. Due to the fact that S100B can have both benefic