Copper Deficiency and the Central Nervous System

DiPaolo, Ronald; Kanfer, Julian N.; Newberne, Paul M.

doi:10.1097/00005072-197404000-00003

Cited by 57 publications

(3 citation statements)

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“…Similarly, the rats fed with an iron-deficient diet showed decreased brain iron content and altered myelin composition, with a 30% decrease in cholesterol in the brain white matter [ 82 ]. Myelin pathology, including demyelination, delayed myelination, and subsequent cavitation of the white matter, has also been found in copper-deficient animals [ 83 , 84 ]. These deficiencies can be partially reversed by subsequent copper diet supplements [ 85 ].…”

Section: Molecular Basis Underlying Myelin Degeneration During Ad Pro...mentioning

confidence: 99%

Myelin Pathology in Alzheimer's Disease: Potential Therapeutic Opportunities

2024

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Alzheimer's disease (AD) is an age-related neurodegenerative disease characterized by memory loss and cognitive decline. Despite significant efforts over several decades, our understanding of the pathophysiology of this disease is still incomplete. Myelin is a multi-layered membrane structure ensheathing neuronal axons, which is essential for the fast and effective propagation of action potentials along the axons. Recent studies highlight the critical involvement of myelin in memory consolidation and reveal its vulnerability in various pathological conditions. Notably, apart from the classic amyloid hypothesis, myelin degeneration has been proposed as another critical pathophysiological feature of AD, which could occur prior to the development of amyloid pathology. Here, we review recent works supporting the critical role of myelin in cognition and myelin pathology during AD progression, with a focus on the mechanisms underlying myelin degeneration in AD. We also discuss the complex intersections between myelin pathology and typical AD pathophysiology, as well as the therapeutic potential of pro-myelinating approaches for this disease. Overall, these findings implicate myelin degeneration as a critical contributor to AD-related cognitive deficits and support targeting myelin repair as a promising therapeutic strategy for AD.

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Section: Molecular Basis Underlying Myelin Degeneration During Ad Pro...mentioning

confidence: 99%

Myelin Pathology in Alzheimer's Disease: Potential Therapeutic Opportunities

2024

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“…A similar state can be produced by raising laboratory animals on a copper-deficient diet, mating them, and maintaining the offspring on the deficient diet after weaning. Such animals have marked underdevelopment of myelin (Everson et al, 1968), status spongiosus (Carleton and Kelly, 1969), significant decreases in sulfatide and cerebroside (di Paolo et al, 1974), and a reduction in 2',3'cyclic nucleotide 3'-phosphohydrolase (Prohaska and Wells, 1974). The last workers also observed a profound decrease in cerebellar cytochrome c oxidase activity and decreased norepinephrine, and suggested that the copper-deficient animal may be a model for Menkes' steely hair disease in the human infant, which is also characterized by decreased myelin and reduced cytochrome c oxidase.…”

Section: Other Deficienciesmentioning

confidence: 99%

Myelin

1977

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“…One aspect of CNS trauma that until recently was relatively understudied is investigation of the elemental changes that occur, especially those of diffusible ions (Cl – , K + , Ca 2+ ) and transition metals (Fe, Cu, Zn). The CNS is highly enriched in transition metal ions, including iron, copper, and zinc, which serve essential roles for neurological function as enzymatic cofactors and contribute to protein modification, neurotransmitter synthesis, myelination, , regulation of rest–activity cycles, and maintenance of redox homeostasis . In addition to transition metal ions, the brain also contains high levels of diffusible ions, such as Ca 2+ , K + , and Cl – , the movement of which is responsible for generation of electric currents associated with action potentials during neuronal signaling. , Therefore, understanding how the levels of diffusible ions change after injury may provide insight into mechanisms through which secondary damage prolongs tissue recovery.…”

Section: Introductionmentioning

confidence: 99%

Elemental Mapping in a Preclinical Animal Model Reveals White Matter Copper Elevation in the Acute Phase of Central Nervous System Trauma

Evans,

Egid,

Mamsa

et al. 2023

ACS Chem. Neurosci.

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Understanding the chemical events following trauma to the central nervous system could assist in identifying causative mechanisms and potential interventions to protect neural tissue. Here, we apply a partial optic nerve transection model of injury in rats and use synchrotron X-ray fluorescence microscopy (XFM) to perform elemental mapping of metals (K, Ca, Fe, Cu, Zn) and other related elements (P, S, Cl) in white matter tracts. The partial optic nerve injury model and spatial precision of microscopy allow us to obtain previously unattained resolution in mapping elemental changes in response to a primary injury and subsequent secondary effects. We observed significant elevation of Cu levels at multiple time points following the injury, both at the primary injury site and in neural tissue near the injury site vulnerable to secondary damage, as well as significant changes in Cl, K, P, S, and Ca. Our results suggest widespread metal dyshomeostasis in response to central nervous system trauma and that altered Cu homeostasis may be a specific secondary event in response to white matter injury. The findings highlight metal homeostasis as a potential point of intervention in limiting damage following nervous system injury.

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Copper Deficiency and the Central Nervous System

Cited by 57 publications

References 0 publications

Myelin Pathology in Alzheimer's Disease: Potential Therapeutic Opportunities

Myelin Pathology in Alzheimer's Disease: Potential Therapeutic Opportunities

Myelin

Elemental Mapping in a Preclinical Animal Model Reveals White Matter Copper Elevation in the Acute Phase of Central Nervous System Trauma

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