Abstract
Hemoglobin (Hb) has been shown to be expressed within dopaminergic neurons and to have a role in maintaining iron and mitochondrial homeostasis. In Parkinson’s disease tissues, Hb has been localized to the mitochondrion. Though heme synthesis occurs within the mitochondria, the localization of Hb to this organelle has only recently been described. It is now important to understand whether Hb expression is protective or is a part of the neurodegenerative process. It is possible that the accumulation of neuronal or mitochondrial Hb is initially protective, but over many decades causes pathology. Studying Hb in neurons can give insight into the iron accumulation seen in the brain and the potential role of alpha-synuclein as a ferrireductase. In this review, we discuss the interactions of neuronal and mitochondrial Hb with other proteins and its possible role in pathways relevant to Parkinson’s disease.
Highlights
Hemoglobin (Hb) has been shown to be expressed within dopaminergic neurons and to have a role in maintaining iron and mitochondrial homeostasis
We postulate here that Hb has an intraneuronal role in contributing to the changes in oxidative status and mitochondrial dysfunction that have been associated with PARKINSON’S DISEASE (PD)
It has been demonstrated that heme is present within neurons, and that heme synthesis declines with age.[20,21]
Summary
Hemoglobin (Hb) has been shown to be expressed within dopaminergic neurons and to have a role in maintaining iron and mitochondrial homeostasis. Much more recently, imaging technology efforts have revealed a “swallow tail” hallmark that is proposed to change in PD.[2] It is always hoped that newer technologies can produce better solutions and markers for PD This neurodegeneration has a recognizable presentation, which can be apparent to the trained neurologist allowed consistent follow-up. There is gathering evidence that Hb levels within the brain affect the risk of developing neurodegenerative diseases including PD.[11,12,13,14,15] Reports associate Hb and neuronal Hb levels with Alzheimer’s disease, dementia with Lewy bodies, age-associated cognitive decline, and argyrophilic grain disease.[10] We postulate here that Hb has an intraneuronal role in contributing to the changes in oxidative status and mitochondrial dysfunction that have been associated with PD
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