Suzanne de la Monte, a neuropathologist at Brown University, has been working on these phenomena in humans and rats. When she blocked the path of insulin to rats’ brains, their neurons deteriorated, they became physically disoriented and their brains showed all the signs of Alzheimer’s. The fact that Alzheimer’s can be associated with low levels of insulin in the brain is the reason why increasing numbers of researchers have taken to calling it Type 3 diabetes, or diabetes of the brain.
Alzheimer's Disease is Type 3 Diabetes: Evidence from Human Studies
This hypothesis was directly investigated by first examining postmortem cases of advanced AD and determining if the neurodegeneration was associated with significant abnormalities in the expression of genes encoding insulin, IGF-1, and IGF-2 peptides, their receptors, and downstream signaling mechanisms.5 In that study, we demonstrated advanced AD to be associated with strikingly reduced levels of insulin and IGF-1 polypeptide and receptor genes in the brain (Figure 1). In addition, all the signaling pathways that mediate insulin and IGF-1-stimulated neuronal survival, tau expression, energy metabolism, and mitochondrial function were perturbed in AD. This study carries additional significance because it established that, like all other pancreatic and intestinal polypeptide genes, the insulin gene was also expressed in the adult human brain. Moreover, the results taught us that endogenous brain deficiencies in insulin, IGF-1, IGF-2, and their corresponding receptors, in the absence of T2DM or obesity, could be linked to the most common form of dementia-associated neurodegeneration in the Western hemisphere. Since the abnormalities identified in the brain were quite similar to the effects of T1DM or T2DM (though none of the patients had either of these diseases), including abnormalities in IGFs,81–83 which are important for islet cell function,84,85 we proposed the concept that AD may represent a brain-specific form of diabetes mellitus and coined the term “type 3 diabetes.”
Well now you make me feel bad. You were acting like an internet troll, so I treated you like one. Had you actually lead with a rational scientific discussion then I would have treated you becoming of that as well.
On the internet it's difficult to tell, when the poster provides no reasoning, evidence, citations, or general educational demeanor. Perhaps lead with data next time :)
You don't want to follow me? Okay. Thats up to you, I don't ask for followers. I will keep doing my thing either way, as well as I can (which may or may not be good at all, but it's my best.)
My apologies for being overly defensive as well. I should not have jumped to conclusions.
I'm just trying to summarize articles to the best of my ability. Provide constructive additions and I will do everything I can to help them get exposure on the post. I am by no means a subject expert in all of the papers I discuss (enzymology yes, every disease ever... Nope) so I assume I will not be perfectly accurate by nature. Hopefully I can do better then say... CNN.
No, it's not.
You have a lot to learn junior. :)
Suzanne de la Monte, a neuropathologist at Brown University, has been working on these phenomena in humans and rats. When she blocked the path of insulin to rats’ brains, their neurons deteriorated, they became physically disoriented and their brains showed all the signs of Alzheimer’s. The fact that Alzheimer’s can be associated with low levels of insulin in the brain is the reason why increasing numbers of researchers have taken to calling it Type 3 diabetes, or diabetes of the brain.
Alzheimer's Disease is Type 3 Diabetes: Evidence from Human Studies
This hypothesis was directly investigated by first examining postmortem cases of advanced AD and determining if the neurodegeneration was associated with significant abnormalities in the expression of genes encoding insulin, IGF-1, and IGF-2 peptides, their receptors, and downstream signaling mechanisms.5 In that study, we demonstrated advanced AD to be associated with strikingly reduced levels of insulin and IGF-1 polypeptide and receptor genes in the brain (Figure 1). In addition, all the signaling pathways that mediate insulin and IGF-1-stimulated neuronal survival, tau expression, energy metabolism, and mitochondrial function were perturbed in AD. This study carries additional significance because it established that, like all other pancreatic and intestinal polypeptide genes, the insulin gene was also expressed in the adult human brain. Moreover, the results taught us that endogenous brain deficiencies in insulin, IGF-1, IGF-2, and their corresponding receptors, in the absence of T2DM or obesity, could be linked to the most common form of dementia-associated neurodegeneration in the Western hemisphere. Since the abnormalities identified in the brain were quite similar to the effects of T1DM or T2DM (though none of the patients had either of these diseases), including abnormalities in IGFs,81–83 which are important for islet cell function,84,85 we proposed the concept that AD may represent a brain-specific form of diabetes mellitus and coined the term “type 3 diabetes.”
Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2769828/
Lol, not from you. :)
I learn from intelligent, knowledgeable people. Not people spreading disinformation on the internet. Go spend your time with more gullible people.
Excuse me?
you don't need to be rude???
I was trying to help you and your followers????
nothing like showing your true colors, I will not be following you.
Well now you make me feel bad. You were acting like an internet troll, so I treated you like one. Had you actually lead with a rational scientific discussion then I would have treated you becoming of that as well.
On the internet it's difficult to tell, when the poster provides no reasoning, evidence, citations, or general educational demeanor. Perhaps lead with data next time :)
You don't want to follow me? Okay. Thats up to you, I don't ask for followers. I will keep doing my thing either way, as well as I can (which may or may not be good at all, but it's my best.)
I have been following you for a bit.
I spoke out because I felt your post was a bit inaccurate.
My appologies for coming across as a internet troll.
Keep on STEEMING friend!
My apologies for being overly defensive as well. I should not have jumped to conclusions.
I'm just trying to summarize articles to the best of my ability. Provide constructive additions and I will do everything I can to help them get exposure on the post. I am by no means a subject expert in all of the papers I discuss (enzymology yes, every disease ever... Nope) so I assume I will not be perfectly accurate by nature. Hopefully I can do better then say... CNN.