More Is Better.....especially when it's Ginkgo Biloba!

I have shared with all of you on my blog that the dose for ginkgo biloba on the Changing Minds Foundation website is a minimum dose to see results.  I have suggested to all I meet that dose is important and the more you give the more results you will see.  My son, Neal, takes 4 to 5 times his weight in ginkgo.  See below what happens when you do increase the amount of ginkgo your child takes.

Below is an email I got from a parent who recently increased her daughter's ginkgo:

My daughter, Whitney, is 7 and has been on NutriChem’s customized vitamin therapy since July, 2010 where we saw major improvements globally with her.  She was diagnosed with PDD-NOS in October, 2009.  I’ve written about her vitamins under the blog section of our website www.bcdsc.org  As noted she went from no expressive language to finally developing expressive language.  Even though she was on 100 mg per day of gingko biloba her processing seemed to have stuck at 3.  A few weeks ago I attended the AutismOne Conference in Chicago and finally got to meet Dr. Teresa Cody.  After our talks, and her suggestion that I increase the gingko significantly, on May 28th we began increasing Whitney’s Gingko to 220 mg per day (50 mg in morning with custom vitamins, 120 mg at lunch with AOR , and another 50 mg before dinner with custom vitamins).  She weighs 42 lbs.  Within a week her teachers at school were noticing increases in ability and more talking (not always clear but more).  One teacher she has on Friday’s was really amazed at the change she has seen week to week.  In addition, I have noticed that Whitney is sleeping longer in the mornings.  So far no 6 am (or earlier) wake ups. 
On June 7th we increased the dose to  110 mg with breakfast, 120 mg with lunch and 110 mg with dinner (340 mg per day).  On June 10th here is what happened:

I’ve been really puzzled this last year as to why Whitney has still only been able to scribble and draw a few circles (roughly) and nothing else.  At lunch today Whitney was drawing on one of those erasable pads and did this:

Drew two parallel lines with a line across the top and said “house”, then put a line in the middle and said “door”, then drew a line with some curly things on the top to the left of the house and said “tree”, then on the other side drew another tree and said “another tree”, then scribbled the bottom and said “grass”.

This for my darling 7 year old daughter is really significant.   All of it, we believe from ramping up the gingko biloba.  Thank you to all the parents who have been saying how important the gingko can be for our children and to Teresa Cody for suggesting that we should try and significantly increase the dosage for Whitney.

Whitney’s teachers, the school aids and other students are all noticing that she is functioning better, not just cognitively but also better co-ordination on the playground and the gym.
We are really impressed and so thankful for Teresa Cody.  It’s unfortunate that Teresa did not get an opportunity to speak at the AutismOne Conference, however, we are very much looking forward to having her on our Cruise and I look forward to hearing more about Gingko and Prozac.  Hopefully she will be speaking in a city close to where I live before the Cruise as I’d like to hear all of her talk.
Best regards,
Rosalie Newell-Wagner
2013 Down Syndrome Cruise Conference
http://www.rosalienewellwagner.cruiseshipcenters.com/Promotions.aspx

New Imaging Shows Down Syndrome Is Slammed With Alzheimer's and We Can See It

Note: My comments in Pink and important STUFF Highlighted

Reported This Week:

Brain scan identifies patterns of plaques and tangles in adults with Down syndrome

		IMAGE: This is a representative PET-FDDNP brain scans of study subjects. Control subject shows minimal binding compared with other subjects. The older Down syndrome (DS) subject shows higher binding than the... Click here for more information.

In one of the first studies of its kind, UCLA researchers used a unique brain scan to assess the levels of amyloid plaques and neurofibrillary tangles — the hallmarks of Alzheimer's disease — in adults with Down syndrome.

Published in the June edition of the Archives of Neurology, the finding may offer an additional clinical tool to help diagnose dementia in adults with Down syndrome, a genetic disorder caused by the presence of a complete or partial extra copy of chromosome 21.

Adults with this disorder develop Alzheimer's-like plaque and tangle deposits early, often before the age of 40. Previously, the only way to physically detect these abnormal proteins in this population was through an autopsy.

Over the last decade, methods for identifying and imaging the neuropathology of Alzheimer's disease in living patients have been developed. UCLA researchers have created a chemical marker called FDDNP that binds to both plaque and tangle deposits, which can then be viewed through a positron emission tomography (PET) brain scan, providing a "window into the brain." Using this method, researchers are able to pinpoint where in the brain these abnormal protein deposits are accumulating.

Due to individual variability and difficulty in obtaining baseline levels of cognitive function in adults with Down syndrome, such imaging may be useful in helping to diagnose dementia, say researchers.

"Neuroimaging may be a helpful tool in assessing and tracking plaque and tangle development over time in this population," said the study's senior author, Dr. Gary Small, a professor at the Semel Institute for Neuroscience and Human Behavior at UCLA who holds UCLA's Parlow-Solomon Chair on Aging. "Early detection can also lead to earlier interventions and treatments, often before symptoms begin." 

 This is great news. Next question what can we use and when can we use it? 

For this study, researchers administered the FDDNP chemical marker intravenously and then performed PET brain scans on 19 non-demented adults with Down syndrome (average age 37), 10 healthy controls (average age 43) and 10 patients with Alzheimer's disease (average age 66).

I don't know about you but average age of 37 is not very old.

Analysis found significantly higher binding levels of the chemical marker in participants with Down syndrome in all brain regions, when compared with healthy controls. Compared with Alzheimer's disease patients, subjects with Down syndrome showed significantly higher binding levels in the parietal and frontal regions — areas involved in memory, behavior and reasoning.

"The higher level of plaques and tangles may be reflecting the early and extensive accumulation of these deposits seen in individuals with Down syndrome," Small said.

The researchers also discovered significant associations between increased age in those with Down syndrome and higher FDDNP binding values in the parietal, lateral temporal and frontal regions.

"This is one of the first times we've been able to visualize the neuropathology occurring in the living brains of adults with Down syndrome," said study author Dr. Jorge R. Barrio, a professor of molecular and medical pharmacology at the David Geffen School of Medicine at UCLA who holds UCLA's Plott Chair in Gerontology. "The age-related patterns and regional distribution of the plaques and tangles were consistent with the types of deposits that could only be identified previously through an autopsy."

While the FDDNP brain scans didn't differentiate between the two types of abnormal proteins, the areas of accumulation were consistent with earlier autopsy study findings, which had shown that while plaque and tangle pathologies are the same in both Down syndrome and Alzheimer's disease, the deposit patterns are different.

Autopsy studies have also shown that all adults with Down syndrome eventually develop these accumulations of amyloid plaques and tau tangles. But rather than experiencing memory decline and other cognitive losses, as is common with Alzheimer's, aging Down syndrome patients tend to develop behavioral problems.

[37 years old is not eventually]

I can't even comment on the ludicrous description that   DS don't experience memory decline. You can't lose what you don't have. 

As part of the study, researchers performed cognitive and behavioral assessments of the Down syndrome subjects to see if FDDNP binding levels correlated with assessment results. They found several positive correlations with behavior abnormalities associated with these brain changes, including indifference and inappropriateness.

Oh great what is inappropriateness????

"We found that the behavioral changes in the subjects with Down syndrome correlated with neurological changes in related areas of the brain consistent with the level of FDDNP binding levels to the abnormal proteins," Small said.

They found the correlation between neurological changes and behavioral changes. This means the behavioral changes are a PHYSICAL Change in the brain. It has nothing to do with motivation or desire. It is not purposeful actions. The patient with Down Syndrome is literally crumbling from the inside out.

Small noted that cognitive skills in people with Down syndrome vary considerably and may not have been captured completely in the assessment, which primarily measured memory function. Larger future studies will compare other cognitive tests with FDDNP binding values, he said.

In addition, researchers plan to determine the relative benefits of different forms of PET imaging using various chemical markers, including FDDNP.

###

This study was supported by the National Institutes of Health and the U.S. Department of Energy.

UCLA owns three U.S. patents on the FDDNP chemical marker. The Office of Intellectual Property at UCLA is actively seeking a commercial partner to bring this promising technology to market.

Small, Barrio and study author S.C. Huang are among the inventors. Disclosures are listed in the full study.

Additional UCLA study authors include Linda D. Nelson, Prabha Siddarth, Vladimir Kepe, S.C. Huang and Kevin E. Scheibel.

For more news, visit the UCLA Newsroom and UCLA News|Week and follow us on Twitter.

So what can we do with this information? Should we take action today or wait until we see the eventual (average age 37) decline?

Choline Part 2

Tomorrow we will get back to the green tea extract and DYRK1 A gene because there are more issues to discuss but today let's look at one little study that showed positive results for the Down syndrome mouse.
Here is the study abstract:
Behav Neurosci. 2010 Jun;124(3):346-61.


Perinatal choline supplementation improves cognitive functioning and emotion regulation in the Ts65Dn mouse model of Down syndrome.
Moon J, Chen M, Gandhy SU, Strawderman M, Levitsky DA, Maclean KN, Strupp BJ.
Division of Nutritional Sciences, Cornell University, Ithaca, NY 14853, USA.

Abstract

In addition to mental retardation, individuals with Down syndrome (DS) also develop the neuropathological changes typical of Alzheimer's disease (AD) and the majority of these individuals exhibit dementia. The Ts65Dn mouse model of DS exhibits key features of these disorders, including early degeneration of cholinergic basal forebrain (CBF) neurons and impairments in functions dependent on the two CBF projection systems; namely, attention and explicit memory. Herein, we demonstrate that supplementing the maternal diet with excess choline during pregnancy and lactation dramatically improved attentional function of the adult trisomic offspring. Specifically, the adult offspring of choline-supplemented Ts65Dn dams performed significantly better than unsupplemented Ts65Dn mice on a series of 5 visual attention tasks, and in fact, on some tasks did not differ from the normosomic (2N) controls. A second area of dysfunction in the trisomic animals, heightened reactivity to committing an error, was partially normalized by the early choline supplementation. The 2N littermates also benefited from increased maternal choline intake on 1 attention task. These findings collectively suggest that perinatal choline supplementation might significantly lessen cognitive dysfunction in DS and reduce cognitive decline in related neurodegenerative disorders such as AD.


PMID: 20528079 [PubMed - indexed for MEDLINE]PMCID: PMC2955960 [Available on 2011/6/1]

They supplemented with choline which crosses the Blood Brain Barrier (protective barrier for the brain) with a transport system. Phosphatidylcholine (PC) passes through the BBB because it  is fat soluble. I'm always thinking about making it as easy as I can for the body. So, my choice of supplementation is PC as opposed to free choline.