Fluoxetine Rescues Quantity and Quality!!!!

Every now and then I plug in 'Down syndrome' into pubmed and let the search engine fly. This morning this is what I found: Brain Pathol. 2012 Jul 23. doi: 10.1111/j.1750-3639.2012.00624.x. Early pharmacotherapy with fluoxetine rescues dendritic pathology in the Ts65Dn mouse model of Down syndrome Guidi S, Stagni F, Bianchi P, Ciani E, Ragazzi E, Trazzi S, Grossi G, Mangano C, Calzà L, Bartesaghi R. Department of Human and General Physiology, University of Bologna, Italy. Abstract DS is a genetic pathology characterized by brain hypotrophy and severe cognitive impairment. Though defective neurogenesis is an important determinant of mental disability, a severe dendritic pathology appears to be an equally important factor. A previous study showed that fluoxetine, a selective serotonin re-uptake inhibitor, fully restores neurogenesis in the Ts65Dn mouse model of DS. The goal of the current study was to establish whether fluoxetine also restores dendritic development. In mice aged 45 days, treated with fluoxetine in the postnatal period P3-P15, we examined the dendritic arbor of the granule cells of the dentate gyrus (DG). The granule cells of trisomic mice had a severely hypotrophic dendritic arbor, fewer spines and a reduced innervation than euploid mice. Treatment with fluoxetine fully restored all these defects. In Ts65Dn mice we found reduced levels of serotonin that were restored by treatment. Results show that a pharmacotherapy with fluoxetine is able to rescue not only the number of granule neurons but also their "quality", in terms of correct maturation and connectivity. These findings strongly suggest that fluoxetine may be a drug of choice for the improvement of the major defects in the DS brain and, possibly, of mental retardation. © 2012 The Authors; Brain Pathology © 2012 International Society of Neuropathology. PMID: 22817700 [PubMed - as supplied by publisher] Say no more......

Early Pharmacotherapy????

An outstanding piece of evidence emerged June of this year. Early treatment of the Down syndrome mouse "restores" cognitive performance. They didn't say "invents" cognitive performance. They say RESTORES. This implies that it is there waiting to be unleashed. And in fact, that is exactly what we observe with the children treated with the CMF protocol. The medicine unveils the awesome person inside.

The medicine used in this study was prozac (fluoxetine generic name). The nerves don't grow or develop properly in the memory area of the brain in Down syndrome. With early treatment with prozac, these DS mice had more normal brain development and had a complete recovery of memory task performance.

All I can say is WOW! We should be dancing on the rooftops and down on our knees thanking God. How easy is this. A known drug with 30 year history and cheap (as low as $3/ month at Walmart).
Watch John (5yo) in action who has been treated with prozac since he was 2 years old:
http://changingmindsfoundation.org/documents/videoblog.html

 Here is an abstract of the study mentioned above:

J Neurosci. 2010 Jun 30;30(26):8769-79.

Early pharmacotherapy restores neurogenesis and cognitive performance in the Ts65Dn mouse model for Down syndrome.
Bianchi P, Ciani E, Guidi S, Trazzi S, Felice D, Grossi G, Fernandez M, Giuliani A, Calzà L, Bartesaghi R.
Department of Human and General Physiology, University of Bologna, I-40126 Bologna, Italy.

Abstract
Down syndrome (DS) is a genetic pathology characterized by intellectual disability and brain hypotrophy. Widespread neurogenesis impairment characterizes the fetal and neonatal DS brain, strongly suggesting that this defect may be a major determinant of mental retardation. Our goal was to establish, in a mouse model for DS, whether early pharmacotherapy improves neurogenesis and cognitive behavior. Neonate Ts65Dn mice were treated from postnatal day (P) 3 to P15 with fluoxetine, an antidepressant that inhibits serotonin (5-HT) reuptake and increases proliferation in the adult Ts65Dn mouse (Clark et al., 2006). On P15, they received a BrdU injection and were killed after either 2 h or 1 month. Results showed that P15 Ts65Dn mice had notably defective proliferation in the hippocampal dentate gyrus, subventricular zone, striatum, and neocortex and that proliferation was completely rescued by fluoxetine. In the hippocampus of untreated P15 Ts65Dn mice, we found normal 5-HT levels but a lower expression of 5-HT1A receptors and brain-derived neurotrophic factor (BDNF). In Ts65Dn mice, fluoxetine treatment restored the expression of 5-HT1A receptors and BDNF. One month after cessation of treatment, there were more surviving cells in the dentate gyrus of Ts65Dn mice, more cells with a neuronal phenotype, more proliferating precursors, and more granule cells. These animals were tested for contextual fear conditioning, a hippocampus-dependent memory task, and exhibited a complete recovery of memory performance. Results show that early pharmacotherapy with a drug usable by humans can correct neurogenesis and behavioral impairment in a model for DS.



PMID: 20592198 [PubMed - indexed for MEDLINE]

Prozac Anyone?

Another study published June 2010 supports the use of Prozac in Down syndrome. Not only does it support the use of Prozac, it indicates Prozac should be started early, probably at birth. Maybe prenatally if you could.
The goal of the study was to see if early pharmacotherapy would improve neurogenesis and cognitive behavior. Guess what? It did.
Neurogenesis is literally what it sounds like. The birth of new neurons or nerves. It is now known that the ability to grow new nerves is a life long affair. At one time, it was believed that higher mammals (humans) did not have the ability to grow new neurons. It has come to light in the research world that we are not above new neurons. In fact, losing the ability to stimulate the growth of new neurons is what leads to depression and other neurodegenerative conditions.
Prozac has been on the market for 30 years. Over 55 million prescriptions have been written. If it had a terrible side effect, we would know. Stomach upset is the most common side effect. I get that from Mexican food.
I'm not making light of using drugs but my point is that weighing the options of degeneration versus regeneration, I'll take the regeneration, thank you.
The study looked at memory and learning in the Down syndrome mouse model. The DS mice did just as well as the typical mice in memory tests.

"These animals were tested for contextual fear conditioning, a hippocampus-dependent memory task, and exhibited a complete recovery of memory performance. Results show that early pharmacotherapy with a drug usable by humans can correct neurogenesis and behavioral impairment in a model for DS."

The abstract and full study is available online "Early Pharmacotherapy Restores Neurogenesis and Cognitive Performance in the Ts65Dn Mouse Model for Down Syndrome"
The thing we should be jumping up and down about is RESTORES COGNITIVE PERFORMANCE!!!!