Alzheimer’s

[cvictorg]

http://www.nytimes.com/2012/03/23/business/drug-dosage-was-approved-despite-warning.html?_r=1&hp

Four months before a best-selling Alzheimer’s drug was set to lose its patent protection, its makers received approval for a higher dosage that extended their exclusive right to sell the drug. But the higher dosage caused potentially dangerous side effects and worked only slightly better than the existing drugs, according to an article published Thursday in the British Medical Journal.

Why Adjust The Dosage on A Useless Drug? | GoozNews

 

[zkt]

Clearly a blatent case of greedy bastards in action. There is no reason in heaven nor hell to think that 23 mg is some kind of magic number of acetycholinesterase inhibitor action. Really, how fuckin stupid do they thingK we ARE?

http://www.nytimes.com/2012/03/23/business/drug-dosage-was-approved-despite-warning.html?_r=1&hp

Four months before a best-selling Alzheimer’s drug was set to lose its patent protection, its makers received approval for a higher dosage that extended their exclusive right to sell the drug. But the higher dosage caused potentially dangerous side effects and worked only slightly better than the existing drugs, according to an article published Thursday in the British Medical Journal.

Why Adjust The Dosage on A Useless Drug? | GoozNews

 

[cvictorg]

Clearly a blatent case of greedy bastards in action. There is no reason in heaven nor hell to think that 23 mg is some kind of magic number of acetycholinesterase inhibitor action. Really, how fuckin stupid do they thingK we ARE?

Question becomes - HOW AND WHY DID THIS GET APPROVED?? As in Watergate we should FOLLOW THE MONEY!!

http://www.nytimes.com/2012/03/23/business/drug-dosage-was-approved-despite-warning.html?_r=1&hp

The drug, Aricept 23, was approved in July 2010 against the advice of reviewers at the Food and Drug Administration.

They noted that the clinical trial had failed to show that the higher dosage — 23 milligrams versus the previous dosages of 5 and 10 milligrams — met its goals of improving both cognitive and overall functioning in people with moderate to severe Alzheimer’s disease.

The single clinical trial of 1,400 patients also found that the larger dosage led to substantially more nausea and vomiting, potentially dangerous side effects for elderly patients struggling with advanced Alzheimer’s disease. The drug was developed by the Japanese pharmaceutical company Eisai but is marketed in the United States in a partnership with Pfizer.

 

[zkt]

The FDA is owned by the drug companies. Maybe the Mexican Cartel could shake them up.

 

[pinkman]

Coconut oil against Alzheimer?

What do you think about this?
Do you think this could really help persons who already show huge signs of dementia?

Coconut Oil Touted as Alzheimer's Remedy - Health & Science - CBN News - Christian News 24-7 - CBN.com

 

[LW64]

Re: Coconut oil against Alzheimer?

Take a look at the Alzheimer's thread.

The medium chain triglycerides extracted from coconut oil - available online as MCT oil - is more effective at providing the ketones needed.

 

[pinkman]

Re: Coconut oil against Alzheimer?

Is MCT oil always from coconut oil? Or is there also MCT oil which isn't made from coconut oil? And is this stuff safe? Does it cause diarrhea or does it pose a risk of arteriosclerosis?

 

[LW64]

Re: Coconut oil against Alzheimer?

Is MCT oil always from coconut oil? Or is there also MCT oil which isn't made from coconut oil? And is this stuff safe? Does it cause diarrhea or does it pose a risk of arteriosclerosis?

Coconut and or Palm oil.

It can cause stomach upset or nausea if you take too much or take it on an empty stomach. A 'dose' is something like a tablespoon.

It contains saturated fats but they pretty much go straight to the liver where they are converted to ketones. These ketones are an alternate fuel for brain cells. Someone who has Alzheimer's has a problem getting glucose into their brain cells for energy and that lack of energy causes the cells to malfunction and eventually die. Ketones bypass that path and provide an alternate source of energy that the brain can operate with.

It can also relieve hot flashes that menopausal women sometimes have. Estrogen helps get glucose into brain cells. When estrogen levels fall during menopause the call goes out for more blood glucose, raising adreniline, increasing body temperature, heart rate, etc.

 

[pinkman]

Re: Coconut oil against Alzheimer?

Hi, does this also work with dementia?

My grandmother is over 95 and she had a rapid onset of dementia over just a few months. She was put on memantine but it raised her blood pressure too high so she had to discontinue it. The doctor said that memantine is the only drug which was suitable for her. He said there are 4 classes of anti-dementia drugs and the other 3 aren't for her because of her other conditions. I am looking for something else which she could try to help her. She notices that something's going on with her and feels helpless and suffers from this.
It's not the case that people with dementia forget stuff and don't care about it.

 

[LW64]

Re: Coconut oil against Alzheimer?

I know its a terrible condition. My mother is 83 and has memory problems. She's been taking one or two tablespoons per day of MCT oil for over a year now. It only seems to keep her mood on the positive side, but otherwise no improvement in memory.

It's impossible to know if it will help at all until you try it. Tell her doctor about it and ramp her up slowly...1/4 tblspn for a few days, then 1/2 tblspn, then 3/4, then 1..up to two or three tblspns a day.

Once she's on a tablespoon you can add in some flaxseed oil (1 teaspoon to 1 tablespoon) and 50 mg EPA to help generate the ketones needed to make this work.


Here's the brand we use:

[ame="http://www.amazon.com/Premium-MCT-Gold-33-8-oz/dp/B000GK11HK/ref=sr_1_3?ie=UTF8&qid=1332650428&sr=8-3"]Amazon.com: Premium MCT Gold 33.8 oz.: Health & Personal Care@@AMEPARAM@@http://ecx.images-amazon.com/images/I/41GVQCF3SVL.@@AMEPARAM@@41GVQCF3SVL[/ame]

 

[Michael Scally MD]

Re: Coconut oil against Alzheimer?

What do you think about this?
Do you think this could really help persons who already show huge signs of dementia?

Coconut Oil Touted as Alzheimer's Remedy - Health & Science - CBN News - Christian News 24-7 - CBN.com

[ame=http://www.youtube.com/watch?v=ZZOR-Qd3QSg]Coconut Oil Touted as Alzheimer's Remedy - CBN.com - YouTube[/ame]

 

[Michael Scally MD]

Talbot K, Wang H-Y, Kazi H, et al. Demonstrated brain insulin resistance in Alzheimer’s disease patients is associated with IGF-1 resistance, IRS-1 dysregulation, and cognitive decline. The Journal of Clinical Investigation. JCI - Demonstrated brain insulin resistance in Alzheimer’s disease patients is associated with IGF-1 resistance, IRS-1 dysregulation, and cognitive decline

While a potential causal factor in Alzheimer’s disease (AD), brain insulin resistance has not been demonstrated directly in that disorder. We provide such a demonstration here by showing that the hippocampal formation (HF) and, to a lesser degree, the cerebellar cortex in AD cases without diabetes exhibit markedly reduced responses to insulin signaling in the IR?IRS-1?PI3K signaling pathway with greatly reduced responses to IGF-1 in the IGF-1R?IRS-2?PI3K signaling pathway. Reduced insulin responses were maximal at the level of IRS-1 and were consistently associated with basal elevations in IRS-1 phosphorylated at serine 616 (IRS-1 pS616) and IRS-1 pS636/639. In the HF, these candidate biomarkers of brain insulin resistance increased commonly and progressively from normal cases to mild cognitively impaired cases to AD cases regardless of diabetes or APOE ?4 status. Levels of IRS-1 pS616 and IRS-1 pS636/639 and their activated kinases correlated positively with those of oligomeric A? plaques and were negatively associated with episodic and working memory, even after adjusting for A? plaques, neurofibrillary tangles, and APOE ?4. Brain insulin resistance thus appears to be an early and common feature of AD, a phenomenon accompanied by IGF-1 resistance and closely associated with IRS-1 dysfunction potentially triggered by A? oligomers and yet promoting cognitive decline independent of classic AD pathology.

 

[zkt]

Dementia can have several causes. Due to the rapid onset, the origion may be vascular; which is not to say that there arent things to do that can improve the future.
Donepizil isnt appropriate, but memantine is.; glutamate antoginist and dopamine agonist.
Other dopamine agonists may be helpful.
There are accounts of folks living healthily into their hundreds.
Then there is the prolonging the agony aspect.
No easy answers here; yet much sympathy.
How far to go is a personal value judgement, I guess.

 

[cvictorg]

http://chronicle.com/article/Losing-It-in-the-Golden-Groves/129543/
Losing It
The lament of an aging professor

http://hansref.blogspot.com/2012/03/alzheimers-and-dementia.html
http://hansref.blogspot.ca/2011/12/methylcobalamin-brain-b12.html
http://hansref.blogspot.ca/2011/12/endogenous-and-dietary-cholesterol-and.html

Causes versus effects: the increasing complexities of Alzheimer’s disease pathogenesis
Amyloid plaques and neurofibrillary tangles are the hallmarks of Alzheimer’s disease and have been the focus of disease etiology and pathogenesis. However, in the larger picture of a complex disease, the precise etiology of the lesions per se, as well as the clinical disease, remain to be defined. In this regard, to date no single process has been identified as a useful target and treatment efforts have shown no meaningful progress. Therefore, alternative ideas that may lead to new and effective treatment options are much needed.

 

[pinkman]

Does coconut oil affect the blood thinning? I'm asking cause my grandmother takes aspirin. Could this interfere with aspirin? I think not but I also don't want to put her on coconut oil when it could be bad for her. What sucks is that when you ask a regular doctor questions like wether one can take fish oil or not because of anticoagulants then usually the doctor will not answer the question but simply say that fish oil doesn't work. I have experienced this time and time again.

 

[Michael Scally MD]

Craddock TJA, Tuszynski JA, Chopra D, et al. The Zinc Dyshomeostasis Hypothesis of Alzheimer's Disease. PLoS ONE 2012;7(3):e33552. PLoS ONE: The Zinc Dyshomeostasis Hypothesis of Alzheimer's Disease

Alzheimer's disease (AD) is the most common form of dementia in the elderly. Hallmark AD neuropathology includes extracellular amyloid plaques composed largely of the amyloid-? protein (A?), intracellular neurofibrillary tangles (NFTs) composed of hyper-phosphorylated microtubule-associated protein tau (MAP-tau), and microtubule destabilization. Early-onset autosomal dominant AD genes are associated with excessive A? accumulation, however cognitive impairment best correlates with NFTs and disrupted microtubules. The mechanisms linking A? and NFT pathologies in AD are unknown. Here, we propose that sequestration of zinc by A?-amyloid deposits (A? oligomers and plaques) not only drives A? aggregation, but also disrupts zinc homeostasis in zinc-enriched brain regions important for memory and vulnerable to AD pathology, resulting in intra-neuronal zinc levels, which are either too low, or excessively high. To evaluate this hypothesis, we 1) used molecular modeling of zinc binding to the microtubule component protein tubulin, identifying specific, high-affinity zinc binding sites that influence side-to-side tubulin interaction, the sensitive link in microtubule polymerization and stability. We also 2) performed kinetic modeling showing zinc distribution in extra-neuronal A? deposits can reduce intra-neuronal zinc binding to microtubules, destabilizing microtubules. Finally, we 3) used metallomic imaging mass spectrometry (MIMS) to show anatomically-localized and age-dependent zinc dyshomeostasis in specific brain regions of Tg2576 transgenic, mice, a model for AD. We found excess zinc in brain regions associated with memory processing and NFT pathology. Overall, we present a theoretical framework and support for a new theory of AD linking extra-neuronal A? amyloid to intra-neuronal NFTs and cognitive dysfunction. The connection, we propose, is based on ?-amyloid-induced alterations in zinc ion concentration inside neurons affecting stability of polymerized microtubules, their binding to MAP-tau, and molecular dynamics involved in cognition. Further, our theory supports novel AD therapeutic strategies targeting intra-neuronal zinc homeostasis and microtubule dynamics to prevent neurodegeneration and cognitive decline.

 

[zkt]

Does coconut oil affect the blood thinning? I'm asking cause my grandmother takes aspirin. Could this interfere with aspirin? I think not but I also don't want to put her on coconut oil when it could be bad for her. What sucks is that when you ask a regular doctor questions like wether one can take fish oil or not because of anticoagulants then usually the doctor will not answer the question but simply say that fish oil doesn't work. I have experienced this time and time again.

No, it doesnt

 

[pinkman]

Cool. I bought native coconut oil. This stuff is really expensive. I paid 4,50 Euros for 200 grams!

But somehow I am very sceptical that this works. How realistic is it to expect that coconut oil could make a difference in a 95 year old senior with dementia? I bet most doctors would laugh about this and say that there simply isn't anything you can do at that age.

 

[zkt]

Cool. I bought native coconut oil. This stuff is really expensive. I paid 4,50 Euros for 200 grams!

But somehow I am very sceptical that this works. How realistic is it to expect that coconut oil could make a difference in a 95 year old senior with dementia? I bet most doctors would laugh about this and say that there simply isn't anything you can do at that age.

You could probably get it on Ebay cheaper.
The difference might show up on a statistical population study. Dont expect much change in the case you mention. Increasing blood floow to the brain might be a more fruitful direction to persue for her.

 

[Michael Scally MD]

Blennow K, Zetterberg H, Rinne JO, et al. Effect of Immunotherapy With Bapineuzumab on Cerebrospinal Fluid Biomarker Levels in Patients With Mild to Moderate Alzheimer Disease. Arch Neurol:archneurol.2012.90. Arch Neurol -- Effect of Immunotherapy With Bapineuzumab on Cerebrospinal Fluid Biomarker Levels in Patients With Mild to Moderate Alzheimer Disease, April 2, 2012, Blennow et al. 0 (2012): archneurol.2012.90v1

Background Given the slow and variable clinical course of Alzheimer disease, very large and extended clinical trials are needed to identify a beneficial clinical effect of disease-modifying treatments. Therefore, biomarkers are essential to prove that an anti–?-amyloid (A?) drug candidate affects both A? metabolism and plaque load as well as downstream pathogenic mechanisms.

Objective To evaluate the effect of the anti-A? monoclonal antibody bapineuzumab on cerebrospinal fluid (CSF) biomarkers reflecting A? homeostasis, neuronal degeneration, and tau-related pathology in patients with Alzheimer disease.

Design Two phase 2, multicenter, randomized, double-blind, placebo-controlled clinical trials of 12-month duration.

Setting Academic centers in the United States (Study 201) and England and Finland (Study 202).

Patients Forty-six patients with mild to moderate Alzheimer disease.

Interventions Patients received either placebo (n = 19) or bapineuzumab (n = 27) in 3 or 4 ascending dose groups.

Main Outcome Measures Changes between end of study and baseline in the exploratory CSF biomarkers A?1-42, A?X-42, A?X-40; total tau (T-tau); and phosphorylated tau (P-tau).

Results Within the bapineuzumab group, a decrease at end of study compared with baseline was found both for CSF T-tau (–72.3 pg/mL) and P-tau (–9.9 pg/mL). When comparing the treatment and placebo groups, this difference was statistically significant for P-tau (P = .03), while a similar trend for a decrease was found for T-tau (P = .09). No clear-cut differences were observed for CSF A?.

Conclusions To our knowledge, this study is the first to show that passive A? immunotherapy with bapineuzumab results in decreases in CSF T-tau and P-tau, which may indicate downstream effects on the degenerative process. Cerebrospinal fluid biomarkers may be useful to monitor the effects of novel disease-modifying anti-A? drugs in clinical trials.