on the home page of this site is an article about exanatide (discovered in the spit of the poisonous gila monster though the chemical is stored in it tail). this drug is used to treat diabetes which stimulates insulin production. it also seems to help protect neurons.
for a while i have been going on about glucose having a beneficial effect, but what if it is the insulin that it stimulates that actually helps?
http://www.hbo.com/alzheimers/science-insulin-in-the-brain.html
"neurons in the brain need glucose to fuel their activities. In fact, PET scans have revealed that when some parts of the brain are engaged in a demanding cognitive task, the neurons in that area metabolize a great deal of glucose.
Within minutes of a meal, insulin is sent to the brain to help neurons absorb and use glucose."
"In addition, insulin regulates the neurotransmitter acetylcholine"
"We realized that every time we raised glucose, we were also raising insulin. And we noticed that the people with higher insulin levels showed the most memory benefit. We wondered if the insulin was enhancing memory, not just the glucose." In a follow-up study, they raised glucose levels, but gave a medication that stopped insulin from being secreted. They found that without insulin, the memory improvement did not occur.
From these early studies, Dr. Craft and her team made two observations: Research volunteers with AD experienced a much higher increase in insulin from the glucose intake than did volunteers without AD, and insulin had to be present for the glucose to help improve memory.
Next, the researchers isolated insulin's effect by raising insulin through an intravenous infusion without raising glucose levels. Memory improved, leading Dr. Craft and her team to conclude that the difference in memory performance is likely the result of increased levels of insulin, not glucose."
"Based on this series of studies, Dr. Craft hypothesized that insulin resistance (with high levels of insulin in the body) paradoxically leads to lower-than-normal levels of insulin in the brain, which results in memory problems. The studies suggest that introducing more insulin to the brain might restore the proper balance of insulin and improve memory. However, more insulin in the rest of the body would be harmful, because it would increase insulin resistance and beta-amyloid levels."
what if people with pd had a low level of insulin in the brain which made the cells vulnerable? Is it possible that exanatide increases the amount of insulin available to the cells?
this is probably all rubbish.
Turnip........ very thought provoking......damn! my teas gone cold. I don't think insulin is synthesised in the brain. Exanatide is an agonist of the glucagon like peptide-1 (GLP-1) receptor of which there are many in the brain. From what I can see of the literature, stimulation of the receptor is suspected to have its neuroprotective effects by inhibiting apoptosis (cell suicide).
sorry about the tea
no, insulin isnt synthesised in the brain unless your pancreas has gone for a wander.
but a sudden increase in insulin might cause a flush of insulin into the brain.
I was thinking that an increase of insulin might be helpful to mitochondrial performance thus preventing cell execution.
http://www.ncbi.nlm.nih.gov/pubmed/20649634
CONCLUSIONS:
Collectively, these results suggest that GLP-1 receptor agonist protects beta cells from hIAPP-induced cell death partially through the activation of AKT pathway and improved mitochondrial function.
i am well out of my depth here and my water wings are punctured so i will have to doggy paddle to the shallow end for a breather.
no, insulin isnt synthesised in the brain unless your pancreas has gone for a wander.
but a sudden increase in insulin might cause a flush of insulin into the brain.
I was thinking that an increase of insulin might be helpful to mitochondrial performance thus preventing cell execution.
http://www.ncbi.nlm.nih.gov/pubmed/20649634
CONCLUSIONS:
Collectively, these results suggest that GLP-1 receptor agonist protects beta cells from hIAPP-induced cell death partially through the activation of AKT pathway and improved mitochondrial function.
i am well out of my depth here and my water wings are punctured so i will have to doggy paddle to the shallow end for a breather.