Chronic inflammation can be a result of microglia. In Alzheimer’s microglia seems to be present around neurons but is not doing its job being a major macrophage. That is cleaning cellular debris and dead neurons. In a direct manner it can activate pro inflammatory cytokines which can bring about widespread inflammation in the brain if somatostatin is low.
Microglia, are targets for the widespread neuropeptide somatostatin and that its receptors can transduce complex signals to microglia.
Microglia is important in the fight against Alzheimer’s disease but not the only player that is failing. Its job is to provide some level of clearance. Low levels of dopamine, promotes this situation as it modulates glia cells.
The stabilization of the internal microtubules is the job of healthy tau, with this stability microtubules direct nutrients and molecules from the cell body to the axon and dendrites. Inside cells of an Alzheimer’s sufferer’s brain, the tau disconnect from the microtubules and stick to each other instead.
Primarily excess amyloid beta and insulin resistance don’t help the health of tau.
Other glia cells that support neurons which are compromised by low dopamine are (mainly) oligodendrocytes, astrocytes.
“They ultimately leave neurons to face excitotoxicity and oxidative stress, Fail to fulfill their homeostatic functions”
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Somatostatin can also be raised by some of the hormones it inhibits. There are a number of factors operating in this illness that can produce this result.
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