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Involvements of Hyperhomocysteinemia in Neurological Disorders
Marika Cordaro1, Rosalba Siracusa2, Roberta Fusco2
1Department of Biomedical, Dental and Morphological and Functional Imaging, University of Messina, Via Consolare Valeria, 98125 Messina, Italy.
Insights
High homocysteine (HCY) levels, known as hyperhomocysteinemia (HHCY), are linked to cardiovascular issues. Emerging research suggests HHCY may also play a significant role in neurodegenerative diseases and neuronal death.
Area of Science:
- Neuroscience
- Biochemistry
- Pathology
Background:
- Homocysteine (HCY) is an amino acid byproduct of protein breakdown.
- Elevated HCY levels define hyperhomocysteinemia (HHCY), a condition primarily associated with arterial damage and cardiovascular disease.
- The connection between HHCY and brain disorders remains largely unexplored.
Purpose of the Study:
- To review the current understanding of hyperhomocysteinemia's potential role in neurodegenerative diseases.
- To explore the mechanisms linking HHCY to brain pathology.
Main Methods:
- Literature review of studies investigating homocysteine metabolism and neurodegeneration.
- Analysis of research on the impact of altered methylation and redox potentials on neuronal function.
Main Results:
- Alterations in HCY metabolism or deficiencies in folate/vitamin B12 can disrupt cellular processes.
- These disruptions include altered calcium influx and accumulation of amyloid and tau proteins.
- A cascade of events, including apoptosis and neuronal death, can result from these changes.
Conclusions:
- Hyperhomocysteinemia is increasingly implicated in the pathogenesis of neurodegenerative conditions.
- Further research is warranted to fully elucidate the mechanisms and therapeutic implications of HHCY in brain health.
Abstract:
Homocysteine (HCY), a physiological amino acid formed when proteins break down, leads to a pathological condition called hyperhomocysteinemia (HHCY), when it is over a definite limit. It is well known that an increase in HCY levels in blood, can contribute to arterial damage and several cardiovascular disease, but the knowledge about the relationship between HCY and brain disorders is very poor. Recent studies demonstrated that an alteration in HCY metabolism or a deficiency in folate or vitamin B12 can cause altered methylation and/or redox potentials, that leads to a modification on calcium influx in cells, or into an accumulation in amyloid and/or tau protein involving a cascade of events that culminate in apoptosis, and, in the worst conditions, neuronal death. The present review will thus summarize how much is known about the possible role of HHCY in neurodegenerative disease.
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