The majority of epilepsies are developmental disorders that start in childhood. But there is a large minority that starts in late adulthood. And increasingly, researchers are suspecting that such epilepsies share mechanisms with dementia. Summarizing the highlights of epilepsy research presented at the recent Annual Congress of the European Academy of Neurology (EAN), Aleksandar Ristic told his audience that the biggest epilepsy story out of the Congress was “not a drug, but it was a reframing.”

In Alzheimer’s disease (AD), 17β-HSD10 and CDK5/p25 contribute to neuronal dysfunction through distinct but interconnected pathways involving mitochondrial impairment and tau-mediated neurodegeneration, supporting their potential as complementary therapeutic targets.

Researchers from Capital Medical University in Beijing, China, aimed to develop novel antidepressant compounds based on the monoaminergic mechanisms of classical antidepressant drugs and the therapeutic potential of 5-HT1A receptor activation.

At the 2026 World Congress of Neuropsychopharmacology (CINP), held in Glasgow June 26-29, 2026, researchers from Japan’s National Center of Neurology and Psychiatry (NCNP) showcased how human organoid technologies are reshaping the study of neurodevelopmental vulnerability, addiction and psychiatric disorders.

Spinal cord traumatic injury can lead to loss of motor function and progressive development of muscle spasticity and rigidity. Researchers from the University of California San Diego and collaborating institutions investigated a novel gene-delivery-based antispasticity strategy.

Neurodegenerative disorders such as Alzheimer’s disease (AD) and frontotemporal dementia are characterized by the accumulation of hyperphosphorylated tau protein, forming neurofibrillary tangles, ultimately leading to synaptic dysfunction and cognitive decline.