Amazing stuff! Good news!
"... But the mechanisms behind age-related inflammation are not well understood. In a study published today (January 20) in Nature, researchers show that older immune cells have a defect in metabolism that when corrected in a mouse model of Alzheimer’s disease can decrease inflammation and restore cognitive function. ...
COX-2 activation is the first step in the production of a lipid called prostaglandin E2 (PGE2), which can bind to one of its receptors, EP2, on immune cells and promote inflammation. To plug up the pathway, [researchers have] shown that deleting the EP2 receptor in mouse macrophages and brain-specific microglia—the cells normally responsible for detecting and destroying immune invaders and cellular debris—reduces inflammation and increases neuronal survival in response to both a bacterial toxin and a neurotoxin. ... "
COX-2 activation is the first step in the production of a lipid called prostaglandin E2 (PGE2), which can bind to one of its receptors, EP2, on immune cells and promote inflammation. To plug up the pathway, [researchers have] shown that deleting the EP2 receptor in mouse macrophages and brain-specific microglia—the cells normally responsible for detecting and destroying immune invaders and cellular debris—reduces inflammation and increases neuronal survival in response to both a bacterial toxin and a neurotoxin. ... "
"... However, the underlying mechanisms that initiate and sustain maladaptive inflammation with ageing are not well defined. Here we show that in ageing mice myeloid cell bioenergetics are suppressed in response to increased signalling by the lipid messenger prostaglandin E2 (PGE2), a major modulator of inflammation. In ageing macrophages and microglia, PGE2 signalling through its EP2 receptor promotes the sequestration of glucose into glycogen, reducing glucose flux and mitochondrial respiration. This energy-deficient state, which drives maladaptive pro-inflammatory responses, is further augmented by a dependence of aged myeloid cells on glucose as a principal fuel source. In aged mice, inhibition of myeloid EP2 signalling rejuvenates cellular bioenergetics, systemic and brain inflammatory states, hippocampal synaptic plasticity and spatial memory. ...
Our study suggests that cognitive ageing ... can be reversed by reprogramming myeloid glucose metabolism to restore youthful immune functions."
Our study suggests that cognitive ageing ... can be reversed by reprogramming myeloid glucose metabolism to restore youthful immune functions."
Here is the underlying research paper:
