A New Strategy in Epilepsy Therapy Through Attenuation of Phosphorylated Tau and Amyloid-beta

Epilepsy is a progressive disorder associated with cognitive decline and worsening of other neuropsychiatric comorbidities, as well as the development of drug resistance. Clinical and experimental evidence has shown a link between epilepsy and neurodegenerative pathways such as tau and amyloid-beta (A(3) proteins. Increased phosphorylation of tau and A(3 is toxic to neurons and can lead to the destabilization of microtubules in the nervous system and axonal dysfunction, resulting in dendrite shrinkage, destabilization of synapses, and ultimately neuronal death. Inhibition or attenuation of tau and A(3 phosphorylation may provide neuroprotective effects and be beneficial in reducing seizures and neurodegeneration. Therefore, anti-amyloid antibodies represent a promising approach, though their use is accompanied by potential benefits and drawbacks. Additionally, anti-tau antibodies hold theoretical potential as an option in epilepsy therapy.