Prozac

Prozac is used as one of the components in the Changing Minds Foundation (CMF) protocol.  Some parents, doctors and advocacy groups find this contentious.  See the Changing Minds Foundation website and look at the research to decide for yourself.

Can Down Syndrome be Treated?

http://www.jneurosci.org/cgi/content/abstract/30/26/8769

The Journal of Neuroscience, June 30, 2010, 30(26):8769-8779; doi:10.1523/JNEUROSCI.0534-10.2010

Early Pharmacotherapy Restores Neurogenesis and Cognitive Performance in the Ts65Dn Mouse Model for Down Syndrome

Patrizia Bianchi,1 Elisabetta Ciani,1 Sandra Guidi,1 Stefania Trazzi,1 Daniela Felice,1 Gabriele Grossi,2 Mercedes Fernandez,3 Alessandro Giuliani,3 Laura Calzà,3 and Renata Bartesaghi1

1Department of Human and General Physiology, University of Bologna, I-40126 Bologna, Italy, 2Center for Applied Biomedical Research, S. Orsola-Malpighi University Hospital, I-40138 Bologna, Italy, and 3BioPharmaNet-Department of Veterinary Morphophysiology and Animal Production, University of Bologna, I-40064 Bologna, Italy

Correspondence should be addressed to Prof. Renata Bartesaghi, Dipartimento di Fisiologia Umana e Generale, Piazza di Porta San Donato 2, I-40126 Bologna, Italy. Email: renata.bartesaghi@unibo.it

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.

Brain Pathol. 2012 Jul 23. doi: 10.1111/j.1750-3639.2012.00624.x. [Epub ahead of print]
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.

Source
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.




This sort of research is disputed by work such as the following:
http://www.frontiersin.org/Evolutionary_Psychology/10.3389/fpsyg.2012.00117/abstract

Primum non nocere: an evolutionary analysis of whether antidepressants do more harm than good
Paul W. Andrews1,2*, J. Anderson Thomson Jr.3,4, Ananda Amstadter2 and Michael C. Neale2
1 Department of Psychology, Neuroscience and Behaviour, McMaster University, Hamilton, ON, Canada
2 Virginia Institute for Psychiatric and Behavioral Genetics, Virginia Commonwealth University, Richmond, VA, USA
3 Counseling and Psychological Services, Student Health, University of Virginia, Charlottesville, VA, USA
4 Institute of Law, Psychiatry and Public Policy, University of Virginia, Charlottesville, VA, USA

Antidepressant medications are the first-line treatment for people meeting current diagnostic criteria for major depressive disorder. Most antidepressants are designed to perturb the mechanisms that regulate the neurotransmitter serotonin – an evolutionarily ancient biochemical found in plants, animals, and fungi. Many adaptive processes evolved to be regulated by serotonin, including emotion, development, neuronal growth and death, platelet activation and the clotting process, attention, electrolyte balance, and reproduction. It is a principle of evolutionary medicine that the disruption of evolved adaptations will degrade biological functioning. Because serotonin regulates many adaptive processes, antidepressants could have many adverse health effects. For instance, while antidepressants are modestly effective in reducing depressive symptoms, they increase the brain’s susceptibility to future episodes after they have been discontinued. Contrary to a widely held belief in psychiatry, studies that purport to show that antidepressants promote neurogenesis are flawed because they all use a method that cannot, by itself, distinguish between neurogenesis and neuronal death. In fact, antidepressants cause neuronal damage and mature neurons to revert to an immature state, both of which may explain why antidepressants also cause neurons to undergo apoptosis (programmed death). Antidepressants can also cause developmental problems, they have adverse effects on sexual and romantic life, and they increase the risk of hyponatremia (low sodium in the blood plasma), bleeding, stroke, and death in the elderly. Our review supports the conclusion that antidepressants generally do more harm than good by disrupting a number of adaptive processes regulated by serotonin. However, there may be specific conditions for which their use is warranted (e.g., cancer, recovery from stroke). We conclude that altered informed consent practices and greater caution in the prescription of antidepressants are warranted.
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Paul Doney,
15 Sep 2009, 18:46
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