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Post by prosper on Aug 17, 2016 7:00:38 GMT -5
This is from a pharmacist friend who also has a small position in MNKD. I think this may be the link to the trial= www.tommorrowstudy.com/?EBlastID=18
New theory for Alzheimer's disease may be caused by excess glucose in the brain which results in plaques and tangles. Inhaled insulin may cross the blood-brain barrier while injected insulin does not. There may be a use for inhaled insulin. See quote from article:
The concept of AD being a sort of diabetes of the brain is being explored elsewhere. In addition to the TOMORROW trial, researchers are investigating an intranasal insulin in the hopes that it will enter the brain and affect metabolism and cognition; injected insulin does not cross the blood-brain barrier, he added.
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Post by liane on Aug 17, 2016 7:28:06 GMT -5
Interesting as this concept is, I don't think it will be an Afrezza application. It's exploiting the very close proximity of the olfactory nerve to the nasal mucosa. The nerve is a direct extension of the brain, and substances do cross the blood brain barrier at this point. You would just need an insulin spray into the nasal cavity, not an inhalation in to the lungs.
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Post by agedhippie on Aug 17, 2016 7:28:15 GMT -5
This is from a pharmacist friend who also has a small position in MNKD. I think this may be the link to the trial= www.tommorrowstudy.com/?EBlastID=18
New theory for Alzheimer's disease may be caused by excess glucose in the brain which results in plaques and tangles. Inhaled insulin may cross the blood-brain barrier while injected insulin does not. There may be a use for inhaled insulin. See quote from article:
The concept of AD being a sort of diabetes of the brain is being explored elsewhere. In addition to the TOMORROW trial, researchers are investigating an intranasal insulin in the hopes that it will enter the brain and affect metabolism and cognition; www.geri.duke.edu/component/content/article/189, he added. TOMMORROW is a study using very low doses of Actos to reduce amyloid deposits and improve AD. This makes sense because there is a research that says amyloid deposits are a key contributor to Type 2. A description is here.
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Post by peppy on Aug 17, 2016 7:47:28 GMT -5
This is from a pharmacist friend who also has a small position in MNKD. I think this may be the link to the trial= www.tommorrowstudy.com/?EBlastID=18
New theory for Alzheimer's disease may be caused by excess glucose in the brain which results in plaques and tangles. Inhaled insulin may cross the blood-brain barrier while injected insulin does not. There may be a use for inhaled insulin. See quote from article:
The concept of AD being a sort of diabetes of the brain is being explored elsewhere. In addition to the TOMORROW trial, researchers are investigating an intranasal insulin in the hopes that it will enter the brain and affect metabolism and cognition; www.geri.duke.edu/component/content/article/189, he added. TOMMORROW is a study using very low doses of Actos to reduce amyloid deposits and improve AD. This makes sense because there is a research that says amyloid deposits are a key contributor to Type 2. A description is here.
12 CLINICAL PHARMACOLOGY 12.1 Mechanism of Action ACTOS is a thiazolidinedione that depends on the presence of insulin for its mechanism of action. ACTOS decreases insulin resistance in the periphery and in the liver resulting in increased insulin-dependent glucose disposal and decreased hepatic glucose output. Pioglitazone is not an insulin secretagogue. Pioglitazone is an agonist for peroxisome proliferator-activated receptor-gamma (PPARγ). PPAR receptors are found in tissues important for insulin action such as adipose tissue, skeletal muscle, and liver. Activation of PPARγ nuclear receptors modulates the transcription of a number of insulin responsive genes involved in the control of glucose and lipid metabolism. In animal models of diabetes, pioglitazone reduces the hyperglycemia, hyperinsulinemia, and hypertriglyceridemia characteristic of insulin-resistant states such as type 2 diabetes. The metabolic changes produced by pioglitazone result in increased responsiveness of insulin-dependent tissues and are observed in numerous animal models of insulin resistance. Because pioglitazone enhances the effects of circulating insulin (by decreasing insulin resistance), it does not lower blood glucose in animal models that lack endogenous insulin.
12.2 Pharmacodynamics Clinical studies demonstrate that ACTOS improves insulin sensitivity in insulin-resistant patients. ACTOS enhances cellular responsiveness to insulin, increases insulin-dependent glucose disposal and improves hepatic sensitivity to insulin. In patients with type 2 diabetes, the decreased insulin resistance produced by ACTOS results in lower plasma glucose concentrations, lower plasma insulin concentrations, and lower HbA1c values. In controlled clinical trials, ACTOS had an additive effect on glycemic control when used in combination with a sulfonylurea, metformin, or insulin [see Clinical Studies (14.2)]. Patients with lipid abnormalities were included in clinical trials with ACTOS. Overall, patients treated with ACTOS had mean decreases in serum triglycerides, mean increases in HDL cholesterol, and no consistent mean changes in LDL and total cholesterol. There is no conclusive evidence of macrovascular benefit with ACTOS or any other antidiabetic medication [see Warnings and Precautions (5.9) and Adverse Reactions (6.1)]. In a 26-week, placebo-controlled, dose-ranging monotherapy study, mean serum triglycerides decreased in the 15 mg, 30 mg, and 45 mg ACTOS dose groups compared to a mean increase in the placebo group. Mean HDL cholesterol increased to a greater extent in patients treated with ACTOS than in the placebo-treated patients. There were no consistent differences for LDL and total cholesterol in patients treated with ACTOS compared to placebo (Table 14). Page 22 of 43 Reference ID: www.accessdata.fda.gov/drugsatfda_docs/label/2011/021073s043s044lbl.pdf
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Post by mnholdem on Aug 17, 2016 7:48:46 GMT -5
This is a site sponsored by Takeda Pharmaceutics, the makers of Actos45. Earlier this year I chatted with CEO Christophe Weber, and learned that the Takeda BoD recently ceased all diabetes R&D, electing to move the company out of the diabetes treatment.
So this study may not have any import as far as Afrezza is concerned, but we mustn't forget that Mannkind's Technosphere pulmonary drug delivery technology is about much more than insulin.
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Post by spiro on Aug 17, 2016 8:07:39 GMT -5
Spiro has noticed that his olfactory nerve appears to working exceptional, but he is not sure if his nasal mucosa along with his neurons are in peak condition. But Spiro is definitely sure that Afrezza continues to help control his diabetes for over 18 month's now, despite some recent weight gain and reduced exercise.
Spiro here, crunch time is coming
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Post by uvula on Aug 17, 2016 8:14:09 GMT -5
The cause of neurodegenerative conditions such as alzheimers are prions. The discovery by Stanley Prusiner was acknowledged with a Nobel prize. Researchers continue to ignore that fact in order to receive funding to remain employed. Expect more money and time wasted demonstrating another false hypothesis. I think you're confusing AD with mad cow disease.
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Post by agedhippie on Aug 17, 2016 10:25:41 GMT -5
This is a site sponsored by Takeda Pharmaceutics, the makers of Actos45. Earlier this year I chatted with CEO Christophe Weber, and learned that the Takeda BoD recently ceased all diabetes R&D, electing to move the company out of the diabetes treatment. So this study may not have any import as far as Afrezza is concerned, but we mustn't forget that Mannkind's Technosphere pulmonary drug delivery technology is about much more than insulin. It may be that they are trying to move Actos out of the diabetes space and into the AD space. My endo tried to get me to take it once but I politely declined.
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Post by kc on Aug 17, 2016 14:24:58 GMT -5
Spiro here, crunch time is coming Is that Crunch time as in Mallomars.
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Post by tayl5 on Aug 17, 2016 17:52:04 GMT -5
The cause of neurodegenerative conditions such as alzheimers are prions. The discovery by Stanley Prusiner was acknowledged with a Nobel prize. Researchers continue to ignore that fact in order to receive funding to remain employed. Expect more money and time wasted demonstrating another false hypothesis. I think you're confusing AD with mad cow disease. There's lots of money that's been wasted on false AD hypotheses, but the prion hypothesis is still open or, in science speak, not disproven. The amyloid-beta that collects into plaques undergoes a conformational change that causes the protein to aggregate, in the same way that conformational shifts in the PrP protein in mad cow disease can propagate from pathogenic proteins to otherwise non-pathogenic proteins. I wouldn't dismiss the other ideas about AD, though. Nobody really knows the answer yet. Hopefully someone will figure it out before I can't remember the question.
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Post by babaoriley on Aug 17, 2016 18:15:18 GMT -5
"It's exploiting the very close proximity of the olfactory nerve to the nasal mucosa." So many people are exploiters these days, nothing surprises me any more. Plenty of it over the years right here on this Board, but, nevertheless, Liane, does that kind of language really belong here? You see the effect it had upon Spiro, he got all worked up!
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Post by peppy on Aug 17, 2016 18:17:43 GMT -5
I think you're confusing AD with mad cow disease. There's lots of money that's been wasted on false AD hypotheses, but the prion hypothesis is still open or, in science speak, not disproven. The amyloid-beta that collects into plaques undergoes a conformational change that causes the protein to aggregate, in the same way that conformational shifts in the PrP protein in mad cow disease can propagate from pathogenic proteins to otherwise non-pathogenic proteins. I wouldn't dismiss the other ideas about AD, though. Nobody really knows the answer yet. Hopefully someone will figure it out before I can't remember the question. Prion Hypothesis.mov www.youtube.com/watch?v=YilqbQ0GRdI
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Post by mnholdem on Aug 17, 2016 19:31:31 GMT -5
"It's exploiting the very close proximity of the olfactory nerve to the nasal mucosa." So many people are exploiters these days, nothing surprises me any more. Plenty of it over the years right here on this Board, but, nevertheless, Liane, does that kind of language really belong here? You see the effect it had upon Spiro, he got all worked up!
Oh, and then liane just had to remind everybody that "The [olfactory] nerve is a direct extension of the brain, and substances do cross the blood brain barrier at this point."
That which is precisely what they DON'T tell you about women's fragrances: it's a blatant attempt to enslave men.
Liane is such an instigator.
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Post by sayhey24 on Aug 17, 2016 20:39:44 GMT -5
This is from a pharmacist friend who also has a small position in MNKD. I think this may be the link to the trial= www.tommorrowstudy.com/?EBlastID=18
New theory for Alzheimer's disease may be caused by excess glucose in the brain which results in plaques and tangles. Inhaled insulin may cross the blood-brain barrier while injected insulin does not. There may be a use for inhaled insulin. See quote from article:
The concept of AD being a sort of diabetes of the brain is being explored elsewhere. In addition to the TOMORROW trial, researchers are investigating an intranasal insulin in the hopes that it will enter the brain and affect metabolism and cognition; injected insulin does not cross the blood-brain barrier, he added. I am not sure about this being a new theory. For many years Alzheimer's has been called Type 3 diabetes by many. A number of years ago I think Matt may have been asked to look at using afrezza which would have been snorted for treating AD. The thought being as a monomer afrezza may provide some advantages over other insulins which were being used as a spray. The snorting device may be something as simple as a straw. I thought it had merit then and I still think it has merit.
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Post by Deleted on Aug 17, 2016 22:09:19 GMT -5
I think you're confusing AD with mad cow disease. There's lots of money that's been wasted on false AD hypotheses, but the prion hypothesis is still open or, in science speak, not disproven. The amyloid-beta that collects into plaques undergoes a conformational change that causes the protein to aggregate, in the same way that conformational shifts in the PrP protein in mad cow disease can propagate from pathogenic proteins to otherwise non-pathogenic proteins. I wouldn't dismiss the other ideas about AD, though. Nobody really knows the answer yet. Hopefully someone will figure it out before I can't remember the question. All hypotheses are open with the possibility of being proven false. No number of experiments can prove a hypothesis true, however one experiment can prove a hypothesis false. Prusiner has demonstrated alzheimers is caused by prions; for doubters I suggest reading his book Madness and Memory.
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