About this Research Topic
Iron is an essential micronutrient in the human diet as it plays significant roles in many important bodily functions, such as oxygen transport, energy production, and as a cofactor for enzyme production. In the nervous system, iron participates in myelination, neurotransmitter synthesis, and receptor expression, being particularly concentrated in catecholaminergic pathways.
Cumulative evidence indicates that iron accumulates in brain regions in typical aging and with the progression of neurodegenerative diseases, such as Parkinson’s and Alzheimer’s diseases, suggesting that iron excess contributes to pathological processes that lead to cell dysfunction and death that are associated with cognitive and functional symptoms.
Aberrant iron homeostasis in late life may be preceded by periods of vulnerability in childhood. Studies have shown that iron overload in the neonatal period persistently disrupts memory in adult and aged rodents, and that iron accumulates in brain regions in animal models of neurotoxicity or genetic animal models of neurodegenerative diseases.
Indiscriminate iron supplementation to infants has been recently considered as a major risk factor for the development of neurodegenerative disorders in the elderly. However, due to the high prevalence of iron deficiency anemia among infants and the known impact of iron deficiency on cognition, iron supplementation during development is praised in many developed and undeveloped countries. Remarkably, some studies suggest that iron supplementation to high hemoglobin, iron-replete infants leads to poorer cognitive performance in childhood and adolescence. Therefore, it is crucial to determine the relationship between iron excess in the brain and cognition across the life course, and cognitive decline associated with aging and neurodegenerative disorders. Furthermore, it is important to establish a safe therapeutic window for iron supplementation during brain development. The present Research Topic aims to gather relevant evidence on cognitive and functional correlates to dietary iron excess or brain iron concentration across the lifespan, and to call attention to this public health challenge of indiscriminate iron supplementation during brain development.
The proposed Research Topic aims to provide an advanced and contemporary overview of:
- the involvement of regional brain iron homeostasis and cognitive and functional impairment;
- the implications of iron supplementation across the life course on cognitive performance;
- the possible role of high brain iron accumulation in neurodevelopmental and neurodegenerative disorders.
Observational and clinical studies of human subjects or patient populations with the study of cognitive or functional assessment are strongly encouraged. Studies of animal models of early life risk or age-related disease, with a special interest in examining potential mechanisms underlying the relation of brain iron concentration and cognitive function, are also welcome. Up-to-date systematic reviews or meta-analysis reports on the topic will be considered.
Cumulative evidence indicates that iron accumulates in brain regions in typical aging and with the progression of neurodegenerative diseases, such as Parkinson’s and Alzheimer’s diseases, suggesting that iron excess contributes to pathological processes that lead to cell dysfunction and death that are associated with cognitive and functional symptoms.
Aberrant iron homeostasis in late life may be preceded by periods of vulnerability in childhood. Studies have shown that iron overload in the neonatal period persistently disrupts memory in adult and aged rodents, and that iron accumulates in brain regions in animal models of neurotoxicity or genetic animal models of neurodegenerative diseases.
Indiscriminate iron supplementation to infants has been recently considered as a major risk factor for the development of neurodegenerative disorders in the elderly. However, due to the high prevalence of iron deficiency anemia among infants and the known impact of iron deficiency on cognition, iron supplementation during development is praised in many developed and undeveloped countries. Remarkably, some studies suggest that iron supplementation to high hemoglobin, iron-replete infants leads to poorer cognitive performance in childhood and adolescence. Therefore, it is crucial to determine the relationship between iron excess in the brain and cognition across the life course, and cognitive decline associated with aging and neurodegenerative disorders. Furthermore, it is important to establish a safe therapeutic window for iron supplementation during brain development. The present Research Topic aims to gather relevant evidence on cognitive and functional correlates to dietary iron excess or brain iron concentration across the lifespan, and to call attention to this public health challenge of indiscriminate iron supplementation during brain development.
The proposed Research Topic aims to provide an advanced and contemporary overview of:
- the involvement of regional brain iron homeostasis and cognitive and functional impairment;
- the implications of iron supplementation across the life course on cognitive performance;
- the possible role of high brain iron accumulation in neurodevelopmental and neurodegenerative disorders.
Observational and clinical studies of human subjects or patient populations with the study of cognitive or functional assessment are strongly encouraged. Studies of animal models of early life risk or age-related disease, with a special interest in examining potential mechanisms underlying the relation of brain iron concentration and cognitive function, are also welcome. Up-to-date systematic reviews or meta-analysis reports on the topic will be considered.
Keywords: Iron, Cognition, Memory, Neurodegenerative Disorders, Iron Supplementation
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
