Diabetes Drug 'significantly Reverses Memory Loss' In Mice With Alzheimer's

GAF

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Diabetes drug 'significantly reverses memory loss' in mice with Alzheimer's

"A drug developed for diabetes could be used to treat Alzheimer's after scientists found it "significantly reversed memory loss" in mice through a triple method of action.
The research, published in Brain Research, could bring substantial improvements in the treatment of Alzheimer's disease through the use of a drug originally created to treat type 2 diabetes.
Lead researcher Professor Christian Holscher of Lancaster University in the UK said the novel treatment "holds clear promise of being developed into a new treatment for chronic neurodegenerative disorders such as Alzheimer's disease.""

"This is the first time that a triple receptor drug has been used which acts in multiple ways to protect the brain from degeneration. It combines GLP-1, GIP and Glucagon which are all growth factors. Problems with growth factor signalling have been shown to be impaired in the brains of Alzheimer's patients."

Thoughts? Comments?
 

Philomath

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Diabetes drug 'significantly reverses memory loss' in mice with Alzheimer's

"A drug developed for diabetes could be used to treat Alzheimer's after scientists found it "significantly reversed memory loss" in mice through a triple method of action.
The research, published in Brain Research, could bring substantial improvements in the treatment of Alzheimer's disease through the use of a drug originally created to treat type 2 diabetes.
Lead researcher Professor Christian Holscher of Lancaster University in the UK said the novel treatment "holds clear promise of being developed into a new treatment for chronic neurodegenerative disorders such as Alzheimer's disease.""

"This is the first time that a triple receptor drug has been used which acts in multiple ways to protect the brain from degeneration. It combines GLP-1, GIP and Glucagon which are all growth factors. Problems with growth factor signalling have been shown to be impaired in the brains of Alzheimer's patients."

Thoughts? Comments?

Breaking it down:
The new drug is actually a triple receptor combining GIP, GLP-1 and Glucagon.

It is now believed that the function of GIP is to induce insulin secretion, which is stimulated primarily by hyperosmolarity of glucose in the duodenum.[10]
GLP-1 has the ability to promote insulin secretion in a glucose-dependent manner. As GLP-1 binds to GLP-1 receptors expressed on the pancreatic β cells, the receptors couples to G-protein subunits and activates adenylate cyclase that increases the production of cAMP from ATP.
cAMP is a second messenger, used for intracellular signal transduction, such as transferring into cells the effects of hormoneslike glucagon and adrenaline.

Glucagon- Glucose is stored in the liver in the form of the polysaccharide glycogen, which is a glucan (a polymer made up of glucose molecules). Liver cells (hepatocytes) have glucagon receptors. When glucagon binds to the glucagon receptors, the liver cells convert the glycogen into individual glucose molecules and release them into the bloodstream, in a process known as glycogenolysis. As these stores become depleted, glucagon then encourages the liver and kidney to synthesize additional glucose by gluconeogenesis.

Insulin sensitivity, deficiency in glucose metabolism...sounds like proof of “Alzheimer’s of the brain” @haidut

Alzheimer Disease (AD) May Be Simply Diabetes Of The Brain

Pehaps someone with more knowledge of diabetes and the aforementioned drugs/chemicals can help determine if this treatment would be beneficial for humans.
 
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GAF

GAF

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Do individuals with Type 2 have a greater incidence of brain diabetes?

Another way of asking is: Do AD individuals usually have type 2 first?
 

haidut

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Breaking it down:
The new drug is actually a triple receptor combining GIP, GLP-1 and Glucagon.

It is now believed that the function of GIP is to induce insulin secretion, which is stimulated primarily by hyperosmolarity of glucose in the duodenum.[10]
GLP-1 has the ability to promote insulin secretion in a glucose-dependent manner. As GLP-1 binds to GLP-1 receptors expressed on the pancreatic β cells, the receptors couples to G-protein subunits and activates adenylate cyclase that increases the production of cAMP from ATP.
cAMP is a second messenger, used for intracellular signal transduction, such as transferring into cells the effects of hormoneslike glucagon and adrenaline.

Glucagon- Glucose is stored in the liver in the form of the polysaccharide glycogen, which is a glucan (a polymer made up of glucose molecules). Liver cells (hepatocytes) have glucagon receptors. When glucagon binds to the glucagon receptors, the liver cells convert the glycogen into individual glucose molecules and release them into the bloodstream, in a process known as glycogenolysis. As these stores become depleted, glucagon then encourages the liver and kidney to synthesize additional glucose by gluconeogenesis.

Insulin sensitivity, deficiency in glucose metabolism...sounds like proof of “Alzheimer’s of the brain” @haidut

Alzheimer Disease (AD) May Be Simply Diabetes Of The Brain

Pehaps someone with more knowledge of diabetes and the aforementioned drugs/chemicals can help determine if this treatment would be beneficial for humans.

Yep, not surprised at all. I don't like that drug though, as they are much safer ways to improve brain insulin sensitivity. Aspirin, niacinamide, and even progesterone have shown much promise in recent human clinical trials. There are studies about that on the forum as well, if you need the specific dosage information.
 

haidut

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Do individuals with Type 2 have a greater incidence of brain diabetes?

Another way of asking is: Do AD individuals usually have type 2 first?

AD sufferers do higher incidence of diabetes II, not just in the brain. There is really no such thing as a localized disease. It is just a localized symptom of metabolic dysfunction. Systemic disease usually precedes these localized symptoms like AD by several decades.
 

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