Galway research aids insight into Alzheimer's disease

RESEARCH led by University of Galway has found evidence that a therapeutic strategy may help to target compromised brain activity in Alzheimer’s disease.

The study focused on nerve cells which routinely limit or restrict activity and messages being sent by the brain, rather than the more conventional approach of therapy for nerve cells which stimulate activity.

Alzheimer’s disease is a chronic progressive neurodegenerative disorder with clinical symptoms including diminished memory and cognitive function. It is the most prevalent cause of dementia, accounting for 60-80% of dementia cases.

The scientists highlighted that symptomatic relief from Alzheimer’s provided by these therapies which target the stimulatory nerve cells is only marginal, and the progression or underlying causes of the disease are not addressed.

Professor Andrea Kwakowsky, Associate Professor of Pharmacology and lead researcher at the School of Medicine, University of Galway, said that the research is looking at the possibility of a therapy which helps to restore a balance in the brain after nerve cells have reacted to Alzheimer's.

“We know, for sure, that the amino acid, GABA, is involved in many important physiological functions of the brain, including being the primary inhibiting factor for nerve cells.

“However, in Alzheimer’s disease, this control that it helps to exert in the brain is compromised, contributing to cognitive decline and memory impairment,” said Professor Kwakowsky.

“Our research is significant in that it demonstrates that if we block this GABA receptor activity in nerve cells, we can reverse Alzheimer-like effects caused by Amyloid beta and improve cognitive performance,” she added.

The team’s research is expanding on a hypothesis that has emerged in recent years, which shifts the focus of therapeutic treatment to the inhibitory side of signalling imbalance in nerve cells, suggesting that targeting the brain’s vulnerability to overstimulation-induced damage can ultimately reduce the impact and death of nerve cells.