Microglias are immune
cells that only arise within the brain. They defend the brain by using cleaning
it of intruders and toxic substances. But, in certain conditions they also can
cause damage. Consequently, they've long been suspected of playing a important
function in neurodegenerative
diseases. As microglia are very long-lived, the scientists have been keen
to find out whether environmental factors change those immune cells a life-time
and what effect this may have on brain health. “Epidemiological research has
proven that infectious diseases and inflammation suffered in the course of
life-time can affect the severity of Alzheimer’s disease much later in life.
Stimulated
immune reaction:
The researchers
investigated how microglia training and tolerance affected the formation of
amyloid plaques in the long term. Such “plaques” are characteristic toxic
deposits that gather within the brains of patients with Alzheimer’s disease. In
a mouse model of Alzheimer’s pathology, the scientists found that trained
microglia amplified the formation of plaques even months after their
immunological memory were triggered, therefore inflicting the disease to become
more intense. In contrast, tolerant microglia decreased plaque load. The
scientists also noticed similar outcomes in a mouse model of stroke.
Consequences
for neurodegenerative diseases?
It’s far possible that
still in humans; inflammatory diseases that generally develop outside the brain
could cause epigenetic reprogramming in the brain. Both infections and diseases
including diabetes or arthritis are related to inflammatory reactions and are
known risk factors for Alzheimer’s disease. The brain’s immunological memory –
epigenetically modified microglia – is one feasible reason behind this impact.
Innate immune memory is
a crucial mechanism of myeloid cell plasticity that takes place in reaction to
environmental stimuli and alters next immune responses. Two kinds of
immunological imprinting may be distinguished—training and tolerance. These are
epigenetically mediated and enhance or suppress next inflammation,
respectively. Whether immune memory occurs in tissue-resident macrophages in
vivo and the way it is able to affect pathology remains largely unknown. Strikingly,
in a mouse model of Alzheimer’s pathology, immune training exacerbates cerebral
ß-amyloidosis and immune tolerance alleviates it; further, peripheral immune
stimulation modifies pathological functions after stroke.
To get the latest
updates and share your thoughts on Neurology- Join us for the advance
Talks/Sessions at Neuron 2018.
No comments:
Post a Comment