#microglial cells

[currentsinbiology]

Phagocytes in the brain—good or bad?

The role of microglial cells in neurodegenerative disease is not fully understood. But new results from researchers in Munich and Basel suggest that stimulation of this arm of the immune system might well delay the onset of such disorders.

Gernot Kleinberger et al. The FTD‐like syndrome causing TREM2 T66M mutation impairs microglia function, brain perfusion, and glucose metabolism, The EMBO Journal (2017). DOI: 10.15252/embj.201796516

A minimal change in the TREM2 gene results in a marked reduction in the phagocytic activity of microglial cells in the brain of mutant mice (green, on the right) relative to the control (yellow and red, on the left). Source: Haass Lab. Credit: Ludwig Maximilian University of Munich      

[sciencenote]

Star Performance

Staying connected is vital for our brain cells. Across a mass of 100 trillion bridges, called synapses, neurons combine to give our brain an unrivalled computing power. But there can be too much of a good thing, and too many active synapses can cause damage to the nervous system. The cognitive and muscular problems caused by Huntingdon’s disease are thought to be triggered in this way. Sufferers produce an abnormal version of a protein, a defect that causes the brain to develop too many stimulatory connections. Stress caused by this is evident in mice whose protein production has been 'switched off' in certain brain areas. Star-shaped cells that respond to brain damage explode into action (activity marked in green) in response to the disruption. Therefore, finding ways to counteract this effect, and allow healthy synapses to grow during development are a top priority for scientists looking for a cure.

Written by Jan Piotrowski

Image by Spencer McKinstry and colleagues

Duke University School of Medicine, USA

Originally published under a Creative Commons Licence (BY 4.0)

Research published in the Journal of Neuroscience, July 2014