Previous studies have shown that applying the anesthetic isoflurane to cultured neural cells can lead to generation of amyloid-beta protein, the key component of senile plaques seen in the brains of Alzheimer's patients. Alzheimer's disease is characterized by plaques within the brain of amyloid-beta protein (A-beta), which is toxic to brain cells.
Researchers have described how the common anesthetic isoflurane may set off a process in which A-beta generation and apoptosis interact with and magnify each other.
In a series of experiments, the researchers first found that applying isoflurane to cultured neural cells increased the activation of the enzyme caspase – a key player in a pathway leading to apoptosis and the development of amyloid-beta protein.
The researchers concluded that caspase activation is essential to the pathway leading to A-beta generation and aggregation.
They also found that isoflurane appears to raise levels of the A-beta-releasing enzymes BACE and gamma secretase and that generation of A-beta plaques further increases isoflurane-induced caspase activation.
The researchers said that even though findings suggest that isoflurane may affect Alzheimer's pathogenesis, these experiments were performed in cultured cells only and more studies would need to be conducted to assess whether this discovery might be relevant to humans.
They also plan to investigate whether other anesthetic agents may produce the same results seen with isoflurane.