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Published on: June 20, 2014
by Alison Kevan for Alzheimer’s Australia Dementia Research Foundation:
New research out of Penn State University suggests that current approaches to develop treatments for Alzheimer’s disease that selectively target amyloid beta have so far proven ineffective in human clinical trials because they may be failing to target the flow-on effects that occur in the brain after amyloid beta plaques appear.
This research was published in the Journal Nature Communications and supports the notion that amyloid beta plaques likely cause the initial damage, but the eventual neurodegeneration seen in Alzheimer’s disease may result from prolonged exposure to a specific neurotransmitter that is released when the brain is injured or diseased.
To give a bit more background, when injury to the brain occurs as a result of either an accident (a traumatic brain injury), a stroke, or the build up of toxic proteins as a result of Alzheimer’s disease and similar conditions, it can activate the brain’s defence and repair mechanism: essentially a chain of neurochemical processes designed to prevent further damage. As part of this chain, a specific type of brain cell called reactive astrocytes, accumulate and produce the neurotransmitter gama-aminobutyric acid (called GABA) at the injured site. GABA is an inhibitory neurotransmitter that plays important roles in normal brain functioning by slowing down neuronal activity in response to certain situations. For example, GABA is released to neutralise the effects of adrenaline during times of nervous tension and stress. When the brain is injured or diseased, GABA can also play a neuroprotective role by reducing inflammation.
The new research has proposed that prolonged release of GABA may have a detrimental impact, however, in suppressing normal neuronal activity.
The research undertaken by Professor Gong Chen and his team at Penn State University studied the brains of deceased humans and mice with Alzheimer’s disease. They found that elevated levels of GABA (and reactive astrocytes) in the dentate gyrus (a part of hippocampus involved in memory processing) contributed to the formation of new episodic memories. The researchers hypothesised that elevated levels of GABA in the dentate gyrus may inhibit normal learning and memory, and thus may cause the memory deficits seen in people with Alzheimer’s disease. Specifically, they believed that GABA could be a new target biomarker in Alzheimer’s disease research.
“Our research shows that the excessively high concentration of the GABA neurotransmitter in these reactive astrocytes is a novel biomarker that we hope can be targeted in further research as a tool for the diagnosis and treatment of Alzheimer’s disease,” Professor Chen said.
Next the researchers examined whether reducing GABA levels would increase neuronal activity and improve their memory capabilities in mice with Alzheimer’s disease. They blocked the transporters (called GAT3/4) that carry and release GABA in reactive astrocytes in the dentate gyrus, and found that the suppression of GABA improved their memory capability.
This result suggest that targeting the GABA neurotransmitter (specifically the GAT3/4 GABA transporter) could be a novel therapeutic approach to reversing the symptoms of Alzheimer’s disease.
“After we inhibited the astrocytic GABA transporter to reduce GABA inhibition in the brains of the Alzheimer’s disease mice, we found that they showed better memory capability than the control Alzheimer’s disease mice. We are very excited and encouraged by this result because it might explain why previous clinical trials failed by targeting amyloid plaques alone.”
These results indicate that therapeutic approaches to Alzheimer’s disease may need to target both the amyloid beta plaques and the ‘downstream’ neurochemical effects of brain injury such as GABA.
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