Immune response to brain infection may trigger Alzheimer’s

ALZHEIMER’S Disease is the most common form of dementia, affecting an estimated 30 million people worldwide. The cause of the condition is unknown, but the prime suspect is amyloid-beta (Aβ), a 42-amino acid peptide which accumulates within neurons to form insoluble structures called senile plaques that are thought to be toxic. Aβ is synthesized in all neurons; it is associated with the cell membrane, and is thought to be involved in cell-to-cell signalling, but its exact role has eluded researchers.

A new study published in the open access journal PLoS One now shows that Aβ is a potent antibiotic that can prevent the growth of a number of disease-causing microbes. The study provides the first evidence of a normal role for Aβ, and also raises the intriguing possibility that Alzheimer’s Disease occurs as a result of the immune system’s response to infection. The findings could make researchers re-think Alzheimer’s, and have implications for how the condition is treated.  

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Optogenetics controls brain signalling and sheds light on Parkinson’s therapy

Optogenetics is a newly developed technique based on a group of light-sensitive proteins called channelrhodopsins, which were isolated recently from various species of micro-organism. Although relatively new, this technique has already proven to be extremely powerful, because channelrhodopsins can be targeted to specific cells, so that their activity can be controlled by light, on a millisecond-by-millisecond timescale.

A group of researchers from Stanford University now report a new addition to the optogenetic toolkit, and demonstrate that it can be used to precisely control biochemical signalling pathways in the mouse brain and to manipulate complex reward-related behaviour. They have also used the existing channelrhodopsins to probe the neural circuitry implicated in Parkinson’s Disease and thus gain a better understanding of why deep brain stimulation is effective in treating the disease.

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