The scientists drew
blood from old mice, whose supply of T cells was depleted, and isolated immune cells.
Plasma from old mice didn't have a strong effect when injected into young mice genetically engineered to lack VCAM1 in certain blood - brain barrier cells.
A new study shows for the first time that gut bacteria
from old mice induce age - related chronic inflammation when transplanted into young mice.
Pancreas
tissue from older mice or from young animals subjected to sleep deprivation exhibited signs of protein misfolding, yet both were able to maintain insulin secretion and control blood sugar levels.
The study found that the microglia cells — the immune cells of the brain — in middle - aged mice already showed altered activity seen in
microglia from older mice.
But
macrophages from older mice acted differently: A-beta's presence incited a big increase in EP2 activity in these cells, resulting in amped - up output of inflammatory molecules and reduced generation of recruiting chemicals and A-beta-digesting enzymes.
The authors show that immune cells, specifically macrophages,
from old mice increase the breakdown of noradrenaline, which is involved in fat breakdown (lipolysis) allowing fat to accumulate.
Several chemical signals that are predominant in young intestinal stem cells were absent or downregulated in stem
cells from older mice, but the researchers zeroed in on the Wnt protein.
They also saw higher levels of TNF and IL - 6, two pro-inflammatory cytokines, in
blood from older mice and blood from older human donors.
Analyzing the DLNs in more details, they found that fewer helper T cells were present, suggesting that these cells
from older mice are less capable of «trafficking» to the lymph nodes.