Researchers have discovered that there are a number of drugs that give cognitive function a boost. These drugs could help fuel our understanding of cognitive disorders, including Alzheimer's disease. Presented in the journal PLoS Biology, the study was funded in part by the MEMSTICK ('Synaptic mechanisms of memory loss: novel cell adhesion molecules as therapeutic targets') project, which received more than EUR 2.9 million under the Health Theme of the EU's Seventh Framework Programme (FP7).
Synapses, which are the neuronal connections in our brain, play a crucial role in our cognitive functions. In particular, it is the synapses' pattern of activity that controls our cognitive functions. Experts say these neuronal connections are dynamic and change in their strength and properties, a process they call synaptic plasticity. Researchers believe this process forms the cellular basis for learning and memory. Some scientists also postulate that alterations in synaptic plasticity mechanisms cause multiple cognitive deficits, including autism, Alzheimer's disease and various forms of mental retardation.
Led by Drs Jose A. Esteban and Shira Knafo from Universidad Autonoma de Madrid and Cesar Venero from Universidad Nacional de Educacion a Distancia in Spain, the researchers identified how this process can be manipulated to give cognitive performance a boost.
The use of a small protein fragment, called a peptide, derived from a neuronal protein involved in cell-to-cell communication can produce a more plastic-like synapse. This peptide (called FGL) triggers a cascade of events within the neuron, which helps facilitate synaptic plasticity.
FGL triggers the insertion of new neurotransmitter receptors into synapses in a region of the brain called the hippocampus, say the researchers, adding this is known to play a role in multiple forms of learning and memory.
Commenting on the results of the study, Dr Esteban says: 'We have known for three decades that synaptic connections are not fixed from birth, but they respond to neuronal activity modifying their strength. Thus, outside stimuli will lead to the potentiation of some synapses and the weakening of others. It is precisely this code of ups and downs what allows the brain to store information and form memories during learning.'
For his part, Dr Knafo remarks: 'These are basic studies on the molecular and cellular processes that control our cognitive function. Nevertheless, they shed light into potential therapeutic avenues for mental disorders where these mechanisms go awry.'
Experts from Denmark, Spain and Switzerland contributed to this study.
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