The Role of Trace Metals in Brain Health

Copper and zinc are essential trace metals that play critical roles in brain function. They contribute to neurotransmitter production, antioxidant defense, and cellular energy metabolism. However, maintaining the right balance is crucial, as both excess and deficiency can have serious consequences for neurological health, including epilepsy, Alzheimer’s disease, and Parkinson’s disease.

Research suggests that copper and zinc imbalances could influence brain excitability, oxidative stress, and neuronal function, potentially increasing the risk of seizures and neurodegenerative conditions.

Copper: Essential Yet Potentially Harmful

Copper is vital for the nervous system, as it helps regulate enzymes, neurotransmitters, and antioxidant defense. However, when copper levels are too high or too low, the consequences can be harmful.

Copper and Seizures

Copper influences the balance of sodium (Na+) and potassium (K+) in the brain, which is crucial for proper electrical signaling. Disrupting this balance can make neurons hyperexcitable, increasing seizure risk.
High copper levels can produce reactive oxygen species (ROS)—harmful molecules that damage brain cells and contribute to oxidative stress, a factor in epilepsy.  Studies suggest that elevated serum copper levels are associated with epilepsy, particularly in middle-aged adults (40-59 years old) (Su et al., 2024).

Copper and Neurodegenerative Diseases

Alzheimer’s disease: Copper accumulation has been linked to plaques and oxidative damage in the brain.  Parkinson’s disease & Multiple Sclerosis: Research suggests that copper dysregulation may contribute to neuronal death and inflammation in these conditions.  Wilson’s disease, a genetic disorder of copper metabolism, leads to toxic copper buildup in the brain and is associated with seizures and epilepsy.

Cuproptosis: A New Form of Copper-Induced Cell Death

Recently, scientists discovered cuproptosis, a unique way cells die due to excess copper. Unlike other forms of cell death, cuproptosis disrupts energy production by interfering with sulfur-containing proteins in the TCA cycle, leading to toxic protein buildup and cell destruction (Tsvetkov et al., 2022).
This process has raised interest in whether cuproptosis plays a role in epilepsy. If excess copper triggers neuron death in a similar way, it could contribute to epileptogenesis—the process by which seizures develop.
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