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25th Annual Southern California Alzheimer's Disease Research Conference Was a Success
Iris L.
Posted: Friday, September 19, 2014 2:28 PM
Joined: 12/15/2011
Posts: 17695


 

 TheAlzheimer's Association of Orange County, CA in conjunction with University of California, Irvine's Institute for Memory Impairments and Neurological Disorders (UCI/MIND) held their 25th Annual Alzheimer's Disease Research Conference.  Several of the presentations were made available on pdf.  I am including a link to the page for the conference.   

 

The conference was on September 12th.  I did not attend this year.  Over 450 doctors, scientists, and families affected by Alzheimer's disease attended.


In regards to one presentation, by Dr. Peter Nelson, the material is difficult to understand, but he is saying that some dementia that is attributed to Alzhemer's disease is actually due to hippocampal sclerosis or cardiovascular disease of the brain.  This probably explains why we see so much variability in the experiences of patients. 

 

 

Here is a link to the page of the pdfs.  

 

2014 Conference Presentations 

http://mind.uci.edu/2014presentations  

 

Iris L. 

 


Mimi S.
Posted: Sunday, September 21, 2014 6:15 PM
Joined: 11/29/2011
Posts: 7027


I wouldn't even attempt to understand it. Lately we are getting lots of theories. Some of them are attempting to figure out that puzzle from the nun's study: Some diagnosed with AD don't have tangles and others without the diagnosis do.
When it's in plain english, I'll attempt to understand it.

Iris L.
Posted: Sunday, September 21, 2014 7:03 PM
Joined: 12/15/2011
Posts: 17695


Mimi, didn't you post an article about hippocampal sclerosis a while ago?  It's another cause for dementia that's not Alzheimer's.   

 

I think the point of his article was that people who look like they have Alzheimer's actually may have something else.

Iris L.
 


Mimi S.
Posted: Monday, September 22, 2014 8:44 AM
Joined: 11/29/2011
Posts: 7027


The article you mention doesn't sound familiar.
We may have to change our definition of dementia as research expands our base knowledge.

Lane Simonian
Posted: Monday, September 22, 2014 10:32 AM
Joined: 12/12/2011
Posts: 5027


The researchers and Iris are correct in most if not all cases: if a person has no plaques and tangles but has cognitive impairment it is likely another form of dementia. 


 

More importantly, a person can have plaques and tangles and have little to no cognitive impairment.  This is possible when a person's antioxidant systems are largely in tact.  When the system is weakened there is mild cognitive impairment.  When the system is broken there is Alzheimer's disease. 


 

For example, people with Down syndrome around the age of 40 almost all have plaques and tangles but only in about 40 percent of the cases do they go on to develop Alzheimer's disease.  An even more striking example is that plaques and tangles are present in children in Mexico City exposed to high levels of air pollution.  They exhibit subtle cognitive impairment, but not Alzheimer's disease. 


 

In the latter case, when the children were fed real cocoa the plaques and tangles disappeared and their cognitive deficits decreased.   


 

Peroxynitrite is the key oxidant in Alzheimer's disease.  Adults with Down syndrome have high levels of myo-inositol which leads to plaques and tangles and peroxynitrites (people with Mild Cognitive Impairment because of high glucose or sodium levels often also have high levels of myo-inositol). Particulate matter and other air pollutants also contribute to the development of plaques, tangles, and peroxynitrites. 


 

Cocoa contains polyphenols that are peroxynitrite scavengers.  Here is a key study. 


 

 2003 Apr 11;140-141:125-32.

Defenses against peroxynitrite: selenocompounds and flavonoids.

Abstract

The inflammatory mediator peroxynitrite, when generated in excess, may damage cells by oxidizing and nitrating cellular components. Defense against this reactive species may be at the level of prevention of the formation of peroxynitrite, at the level of interception, or at the level of repair of damage caused by peroxynitrite. Several selenocompounds serve this purpose and include selenoproteins such as glutathione peroxidase (GPx), selenoprotein P and thioredoxin reductase, or low-molecular-weight substances such as ebselen. Further, flavonoids, such as (-)-epicatechin, which occurs in green tea or cocoa as monomer or in the form of oligomers, can contribute to cellular defense against peroxynitrite.

 

If you inhibit peroxynitrite formation through exercise and a diet high in polyphenols and omega 3-fatty acids (a Mediterranean diet or a diet from India), you delay the onset of Alzheimer's disease.  If you scavenge peroxynitrites (with polyphenols for example), you slow down the progression of the disease.  And if you reverse part of the damage done by peroxynitrites with particular phenolic compounds, you partially reverse the disease (eugenol in various essential oils and ferulic acid, vanillic acid, and syringic acid in panax ginseng, for instance).  The key to effectively treating Alzheimer's disease, I believe, is pairing the right essential oils via aromatherapy (clove, bay laurel, rosemary, nutmeg, lemon balm, etc.) with the right aromatic herbs (ginseng, lemon balm, Angelica archangelic, medical marijuana, for instance).  Moderate exercise and a Mediterranean diet will also help. 

 

Mimi awhile back you had mentioned taking a medication for another condition.  I could not find anything on it and how it might help Alzheimer's disease the first time, but I would like to take another shot at it. 


Lane Simonian
Posted: Monday, September 22, 2014 10:55 AM
Joined: 12/12/2011
Posts: 5027


It just occurred to me that I have read several articles over the last month asking exactly the same question: why do many people have plaques and tangles in their brain but not have Alzheimer's disease?  I don't think they have found the right answer yet, but once they do, the sky is the limit to preventing and treating Alzheimer's disease.  


Here is what is likely the right answer to the question:


The alternate hypothesis...is that Aβ simply represents a bystander or a protector rather than the causative factor of disease (Smith et al., 2002; Lee et al.,20032004b). Notably, all therapeutic studies that have an effect on Aβ levels in cells or animals have shown extremely poor or no efficacy in subsequent clinical trials. This includes indomethacin (Weggen et al., 2001), ibuprofen (Lim et al., 2000), sulindac sulfide (Weggen et al., 2001), a nitric oxide-releasing nonsterodial anti-inflammatory drug (Jantzen et al., 2002), and estrogen (Zheng et al., 2002). Clearly, the alternate hypothesis points to greater therapeutic efficacy by directing efforts to the upstream metabolic and oxidative abnormalities that are what led to Aβ.





Iris L.
Posted: Monday, September 22, 2014 1:09 PM
Joined: 12/15/2011
Posts: 17695


Lane Simonian wrote:

  An even more striking example is that plaques and tangles are present in children in Mexico City exposed to high levels of air pollution.  They exhibit subtle cognitive impairment, but not Alzheimer's disease. 


 

In the latter case, when the children were fed real cocoa the plaques and tangles disappeared and their cognitive deficits decreased.   


 

 

Mimi awhile back you had mentioned taking a medication for another condition.  I could not find anything on it and how it might help Alzheimer's disease the first time, but I would like to take another shot at it. 

 

 

 

 

 

 Lane, was the high levels of air pollution due to lead exposure?  I don't know if lead was removed from gasoline in Mexico.  Lead is known to cause delayed intellectual development in children. 

 

Mimi was treated for myasthenia gravis.  I don't remember the medication she used.

Iris L.

 

 


Myriam
Posted: Monday, September 22, 2014 1:18 PM
Joined: 12/6/2011
Posts: 3326


 "...when the children were fed real cocoa the plaques and tangles disappeared and their cognitive deficits decreased." 

 

Wow, does this mean if we eat dark chocolate it will reduce the plaques and tangles. Running to the store to get some dark (baking) chocolate! I have a vague recollection of a discussion about dark chocolate, and remember buying and eating it, but guess I forgot. :-/ confused 

 

 

 


Lane Simonian
Posted: Monday, September 22, 2014 2:36 PM
Joined: 12/12/2011
Posts: 5027


I got my studies mixed up.  Here is the one for the children in Mexico City:


The effects of cocoa and dark chocolate include improvement of endothelial function, marked reduction in oxidative stress and in the production of pro-inflammatory cytokines, eicosanoids, and in platelet activation (Akita et al., ; Selmi et al., ; Ghosh and Scheepens, ; Monagas et al., ; Panneerselvam et al., ; Spadafranca et al., ). There are significant neuroprotective effects of cocoa flavonols including angiogenesis [increased blood flow], neurogenesis in regions involved in learning and memory [regeneration of neurons], cognition improvement, positive effects on mood, and a significant correlation between chocolate consumption per capita and Nobel laureates (Fisher et al., ; Francis et al., ; Patel and D'Souza,; Scholey et al., ; Field et al., ; Desideri et al., ; Messerli, ; Vauzour, ; Williams and Spencer, ; Nehlig, ). In a meta-analysis review of 1106 subjects examining the short effect of flavonoid-rich cocoa, Shrime et al. () concluded that cocoa consumption significantly improved blood pressure, insulin resistance, lipid profiles and flow-mediated vascular dilatation in adults.

It is worth mentioning that short interventions sometimes fail to support the predicted beneficial effects of flavonols in older adults (Crews et al., ), and some studies have shown positive mood states but not cognitive improvement (Crews et al., ; Pase et al., ), although no such studies have been reported in children. Here, we have reported preliminary evidence of cognitive improvement in children. Although the improvement was marginally significant, still it is impressive that we were able to observe those effects in such a short intervention.


And the cocoa study from this summer:

Pages 643-650
Jun Wang*, Merina Varghese*, Kenjiro Ono, Masahito Yamada, Samara Levine, Nikos Tzavaras, Bing Gong, William J. Hurst, Robert D. Blitzer, Giulio Maria Pasinetti *These authors contributed equally to this work.
Cocoa Extracts Reduce Oligomerization of Amyloid-β: Implications for Cognitive Improvement in Alzheimer’s Disease
Abstract: Background: Alzheimer’s disease (AD) is the most common age-related neurodegenerative disorder, characterized by pathological aggregates of amyloid peptide-β (Aβ) and tau protein. Currently available therapies mediate AD symptoms without modifying disease progression. Polyphenol-rich diets are reported to reduce the risk for AD. Objective: In the present study, we investigated the AD disease-modifying effects of cocoa, a rich source of flavanols, which are a class of polyphenols. We hypothesized that cocoa extracts interfere with amyloid-β oligomerization to prevent synaptic deficits. Methods: We tested the effects of three different cocoa extracts, viz. Natural, Dutched, and Lavado extracts, on Aβ42 and Aβ40 oligomerization, using photo-induced cross-linking of unmodified proteins technique. To assess the effects of cocoa extracts on synaptic function, we measured long term potentiation in mouse brain hippocampal slices exposed to oligomeric Aβ. Results: Our results indicate that cocoa extracts are effective in preventing the oligomerization of Aβ, with Lavado extract being most effective. Lavado extract, but not Dutched extract, was effective in restoring the long term potentiation response reduced by oligomeric Aβ. Conclusion: Our findings indicate that cocoa extracts have multiple disease-modifying properties in AD and present a promising route of therapeutic and/or preventative initiatives.

Dark chocolate in combination with various herbs and aromatheapy

may be helpful in the treatment of Alzheimer's disease.



Mimi S.
Posted: Monday, September 22, 2014 7:32 PM
Joined: 11/29/2011
Posts: 7027


Iris: I doubt you'll find anything, but do give it a try. 

I take huge doses of Mestinon for Myasthenia Gravis. 
And as the first neurologist I asked retorted: the Mestinon is not designed to have any effect on AD. He and my own specialist think there is a possibility that the Mestinon is having an effect on the AD. neither have gotten back to me on any studies. To have both is rare.
My neurologist practices in one of the large teaching hospitals in NYC. I am his only patient with both diseases.
That's one of the reasons I am thrilled by the millions tat have been raised by people dumping buckets on their heads and also sending in money for ALS. The ALS is said to be a first cousin of MG. (Boy, did I luck out!)  And research into the brain is going to help all of us with a neurological disease.

Lane Simonian
Posted: Monday, September 22, 2014 11:01 PM
Joined: 12/12/2011
Posts: 5027


I found a little more this time, but none of it very conclusive.  The following study is for pyridostigmine and mestinon is pyridostigmine bromide. 


 

 1989 Mar-Apr;10(2):199-204.

Acute effects of oral pyridostigmine on memory and cognitive function in SDAT.

Abstract

This study reports the effects of the anticholinesterase pyridostigmine on cognitive function in 15 elderly patients with senile dementia of the Alzheimer type (SDAT). Each patient was given placebo and pyridostigime 60 mg orally four times over 26 hours, with a seven day washout between, using a randomized double-blind cross-over design. There was no significant improvement in cognitive function following placebo or pyridostigmine. We did not perform any preliminary dose-finding trials to find the optimum dose of pyridostigmine, but gave the drug in a predetermined fixed dosage to each patient. We conclude that with this dosage, pyridostigmine did not significantly improve cognitive function more than placebo in this group of elderly patients.

 

There are a few studies suggesting that pyridostigmine bromide especially in combination with stress or environmental toxins actually can have a negative effect on the central nervous system (possibly part of Gulf War Syndrome).   


 

http://www.ncbi.nlm.nih.gov/pubmed/23807240 


Mimi S.
Posted: Tuesday, September 23, 2014 8:53 AM
Joined: 11/29/2011
Posts: 7027


Lane:

This time I have problems not only with the number. Fifteen people  is only a preliminary and the dosage is one little pill over a very short period of time. 

 

Would we judge if Aricept worked by doing the same short period? Hardly.

However, I do wonder what led to the study? What made someone wonder if there was a connection?


Lane Simonian
Posted: Tuesday, September 23, 2014 9:13 AM
Joined: 12/12/2011
Posts: 5027


Two reasons likely: pyridostigmine is an acetylcholinesterase inhibitor and a muscarinic acetylchloline agonist.  One would suspect both actions by increasing acetylcholine levels would help improve short-term memory. But it appears the reverse may be the case.  Certain pesticides also over- activate muscarinic acetylcholine receptors and contribute to memory loss.  Pyridostigmine potentially produces the same result.  I was hoping it might help in the treatment of Alzheimer's disease.  Now its effect appears to be neutral (at least in one very small study) and it may actually increase the risk for Alzheimer's disease.  



 2000 Aug;21(4):541-52.

Muscarinic receptor-mediated pyridostigmine-induced neuronal apoptosis.

Rat cortical cells in culture also underwent apoptosis [cell death] when exposed to pyridostigmine (250 microM for 24 hr), indicating that the pyridostigmine can initiate apoptosis, independent of peripheral mechanisms. Pretreatment of cells with atropine (10 microM) inhibited pyridostigmine-induced apoptosis, confirming the response was mediated by muscarinic receptors. Short term treatment of rats with pyridostigmine (1.85 mg/kg twice daily for 4 days) induced a prolonged apoptotic response, which was evident in rat cortex up to 30 days after the last dose. Active apoptosis persisted, despite recovery of serum ChE [acetylcholinesterase] activity. These in vivo and in vitro observations indicate that pyridostigmine can initiate a prolonged neurodegeneration.

 
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