Up over $4 today. Below copied from IHUB, Fletch
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Posted On: 06/11/2018 1:54:05 PM
Up over $4 today. Below copied from IHUB,
Fletch
Posts by falconer66a on IHUB
Mitochondrial Dysfunction Is the Root Cause of Alzheimer’s
According to the unique Anavex 2-73 mechanism of action, the root, basal cause of at least some Alzheimer’s cases (perhaps most or all), is the incomplete or error-prone folding of essential proteins (enzymes) that modulate and control proper, healthful neuron chemistry. These folding errors occur because the rough endoplasmic reticula, adjacent to and normally touching mitochondria, normally fold proteins into functioning enzymes.
This requires ample concentrations of energy-supplying adenosine triphosphate (ATP), which is synthesized in the mitochondria. In the case of Alzheimer’s, the endoplasmic reticula no longer functionally connect to the mitochondria, restricting normal transport of ATPs into the rough ER. With this deficit, there is insufficient energy to power protein folding. Hence, proteins are made, but they are improperly shaped and can no longer facilitate normal chemical reactions in the neuron. Consequently, toxic molecules are made and no longer removed or destroyed. Beta-amyloids and tau tangles accumulate, disrupting and slowing normal neuron and nerve function. Alzheimer’s symptoms present.
In review (briefly, incompletely), Anavex 2-73 re-connects the rough endoplasmic reticula with adjacent mitochondria, and restores normalized molecular and ion (Ca++) exchanges, allowing proper, normalized protein folding. Consequently, neurons and nerves function normally again.
As a large number of papers on the disease will attest, Alzheimer’s (and most other CNS diseases) is a disease of mitochondrial dysfunction. Anavex 2-73 restores effective ATP synthesis and transport from mitochondria into the rough ER. After that, things work normally.
https://investorshub.advfn.com/boards/read_ms...=141436521
Good Question --- Age and/or Genetics
What causes, then, the mitochondria to no longer function properly? What causes them to no longer connect effectively with endoplasmic reticula? Two probable reasons (and there may be more).
The first is simple age. No one can contest that by middle age, organs and tissues no longer function as well as in the first half of life. Mechanisms weaken. Likewise, in neurons. The structural chemistry holding things, literally, together, weakens. Anavex 2-73 re-connects and supports the otherwise weakened sub-cellular structure in the neuron.
In other cases, particularly with early-onset Alzheimer's, defective genetics prevents full structural architecture and function.
And, as the genomic analyses performed in the Australian trial have apparently discovered, there are specific genetic patterns that correlate very positively with Anavex 2-73 efficacy. The neuron aging process has genetic controlling components, which Anavex Life Sciences Corp has now discovered. With these predictive genomic data, the company will be able to select for the upcoming clinical trial of Anavex 2-73 only participants who have those specific Alzheimer's-prone, Anavex 2-73-favorable genes.
The trial process is now stacked in Anavex's favor. Only those who have Alzheimer's genes open to Anavex 2-73 efficacy will be allowed to participate in the trial. Precise stuff. "Precision medicine."
Ponder, then, who will benefit.
https://investorshub.advfn.com/boards/read_ms...=141436821
How Many Might Anavex Treat?
Good question. What percent of those with Alzheimer’s might Anavex 2-73 effectively and efficiently treat? Presently, unknown, of course.
For a start, presently, the question is, what percent of the Alzheimer’s people in the upcoming clinical trial will be effectively treated? How many will benefit? With the ability to carefully select for the trail only those with Anavex-favorable Alzheimer’s genetics, efficacy rates in the trial should be very high, if not just downright remarkable. With trial results approaching any of that, FDA approval of the drug should be coming forthwith.
Will that mean, then, that Anavex 2-73 will work on only a small fraction of Alzheimer’s patients? If it’s for only 10% with the disease, Anavex Life Sciences Corp will be a success (and our AVXL share prices will be rewarding).
But there is good reason that the drug will help with the successful treatment of a diversity of CNS diseases — including, at least to a degree, Alzheimer’s cases lacking a strong genetic component. Why? Because in all cases the mitochondrial dysfunction I described in a previous post causes the problems. At least to a degree, if not altogether markedly, our drug restores cellular function (“homeostasis”).
Now, for people with advanced cases, where nerve function is significantly disrupted, after several years of debility, the drug may not be able to put things back together. At some point, Alzheimer’s may have incurred permanent, irreparable nerve damage.
But what hasn’t been yet tested or known is the prophylactic abilities of Anavex 2-73, the ability of the administered drug to prevent or reverse the onset of Alzheimer’s and other degenerative CNS diseases. Because of the drug’s unique and powerful mechanism of action, there is every reason to believe it will have profound prophylactic capabilities. Aunt Matilda might be prescribed the drug at the very first sign of memory deficiency. “Doc, I’m forgetting where I left my keys in the house.” “Well then, here, get this prescription filled. Your insurance company will be relieved. In a few weeks, you’ll be remembering all sorts of things. This new Anavex drug is really remarkable.”
Good chance that the biggest, most effective use of Anavex 2-73 will be to prevent or treat the early onset of CNS diseases. Giant global market for such.
https://investorshub.advfn.com/boards/read_ms...=141439457
Fletch
Posts by falconer66a on IHUB
Mitochondrial Dysfunction Is the Root Cause of Alzheimer’s
According to the unique Anavex 2-73 mechanism of action, the root, basal cause of at least some Alzheimer’s cases (perhaps most or all), is the incomplete or error-prone folding of essential proteins (enzymes) that modulate and control proper, healthful neuron chemistry. These folding errors occur because the rough endoplasmic reticula, adjacent to and normally touching mitochondria, normally fold proteins into functioning enzymes.
This requires ample concentrations of energy-supplying adenosine triphosphate (ATP), which is synthesized in the mitochondria. In the case of Alzheimer’s, the endoplasmic reticula no longer functionally connect to the mitochondria, restricting normal transport of ATPs into the rough ER. With this deficit, there is insufficient energy to power protein folding. Hence, proteins are made, but they are improperly shaped and can no longer facilitate normal chemical reactions in the neuron. Consequently, toxic molecules are made and no longer removed or destroyed. Beta-amyloids and tau tangles accumulate, disrupting and slowing normal neuron and nerve function. Alzheimer’s symptoms present.
In review (briefly, incompletely), Anavex 2-73 re-connects the rough endoplasmic reticula with adjacent mitochondria, and restores normalized molecular and ion (Ca++) exchanges, allowing proper, normalized protein folding. Consequently, neurons and nerves function normally again.
As a large number of papers on the disease will attest, Alzheimer’s (and most other CNS diseases) is a disease of mitochondrial dysfunction. Anavex 2-73 restores effective ATP synthesis and transport from mitochondria into the rough ER. After that, things work normally.
https://investorshub.advfn.com/boards/read_ms...=141436521
Good Question --- Age and/or Genetics
What causes, then, the mitochondria to no longer function properly? What causes them to no longer connect effectively with endoplasmic reticula? Two probable reasons (and there may be more).
The first is simple age. No one can contest that by middle age, organs and tissues no longer function as well as in the first half of life. Mechanisms weaken. Likewise, in neurons. The structural chemistry holding things, literally, together, weakens. Anavex 2-73 re-connects and supports the otherwise weakened sub-cellular structure in the neuron.
In other cases, particularly with early-onset Alzheimer's, defective genetics prevents full structural architecture and function.
And, as the genomic analyses performed in the Australian trial have apparently discovered, there are specific genetic patterns that correlate very positively with Anavex 2-73 efficacy. The neuron aging process has genetic controlling components, which Anavex Life Sciences Corp has now discovered. With these predictive genomic data, the company will be able to select for the upcoming clinical trial of Anavex 2-73 only participants who have those specific Alzheimer's-prone, Anavex 2-73-favorable genes.
The trial process is now stacked in Anavex's favor. Only those who have Alzheimer's genes open to Anavex 2-73 efficacy will be allowed to participate in the trial. Precise stuff. "Precision medicine."
Ponder, then, who will benefit.
https://investorshub.advfn.com/boards/read_ms...=141436821
How Many Might Anavex Treat?
Good question. What percent of those with Alzheimer’s might Anavex 2-73 effectively and efficiently treat? Presently, unknown, of course.
For a start, presently, the question is, what percent of the Alzheimer’s people in the upcoming clinical trial will be effectively treated? How many will benefit? With the ability to carefully select for the trail only those with Anavex-favorable Alzheimer’s genetics, efficacy rates in the trial should be very high, if not just downright remarkable. With trial results approaching any of that, FDA approval of the drug should be coming forthwith.
Will that mean, then, that Anavex 2-73 will work on only a small fraction of Alzheimer’s patients? If it’s for only 10% with the disease, Anavex Life Sciences Corp will be a success (and our AVXL share prices will be rewarding).
But there is good reason that the drug will help with the successful treatment of a diversity of CNS diseases — including, at least to a degree, Alzheimer’s cases lacking a strong genetic component. Why? Because in all cases the mitochondrial dysfunction I described in a previous post causes the problems. At least to a degree, if not altogether markedly, our drug restores cellular function (“homeostasis”).
Now, for people with advanced cases, where nerve function is significantly disrupted, after several years of debility, the drug may not be able to put things back together. At some point, Alzheimer’s may have incurred permanent, irreparable nerve damage.
But what hasn’t been yet tested or known is the prophylactic abilities of Anavex 2-73, the ability of the administered drug to prevent or reverse the onset of Alzheimer’s and other degenerative CNS diseases. Because of the drug’s unique and powerful mechanism of action, there is every reason to believe it will have profound prophylactic capabilities. Aunt Matilda might be prescribed the drug at the very first sign of memory deficiency. “Doc, I’m forgetting where I left my keys in the house.” “Well then, here, get this prescription filled. Your insurance company will be relieved. In a few weeks, you’ll be remembering all sorts of things. This new Anavex drug is really remarkable.”
Good chance that the biggest, most effective use of Anavex 2-73 will be to prevent or treat the early onset of CNS diseases. Giant global market for such.
https://investorshub.advfn.com/boards/read_ms...=141439457
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