The Dallas Cowboys Tony Dorsett Is losing His Memory Because Tony Has Neuroblastoma And Gene TDP-43 
Houston, Texas ( AP ) Barron’s Medical Journal Sports was concerned after seeing Tony Dorsett the famous running back for The Dallas Cowboys announced that he was losing his memory. Barron’s
The Gene TDP-43 In Adults And Gene MYCN or CD44 In Kids has shown some amazing results. Neuroblastoma is a malignant (cancerous) tumor that develops from nerve tissue. It usually occurs in infants and children.
Barrons Medical Journal ask Sam Houston Biotech CEO for answers. To our surprise Rose Conrad Sam Houston CEO says that it has been known for years that some football players have a gene called TDP- 43. TAR DNA-binding protein of 43kDa (TDP-43). Genomics is again the key to equalize a patient’s risk. Conrads says new Genomics genetic risk factor for amyotrophic lateral sclerosis, commonly known as ALS or Lou Gehrig's disease.
There is no cure for ALS and the current treatment only slows disease progression. The identification of pathological interactions between ataxin 2 and TDP-43, another ALS-associated disease protein, together with the strong genetic association of ataxin 2 intermediate-length polyQ expansions and ALS, should aid in the development of biomarkers and empower the development of new therapies for this disease.
Barron’s Medical Journal Researched Joshua M. Shulman, M.D., Ph.D. of Laboratory for Integrative Functional Genomics Departments of Neurology and Molecular & Human Genetics Baylor College of Medicine. Their mission is to offer clinical manifestation of neurodegenerative disease is the culmination of a multi-tiered pathogenic cascade that evolves over decades—understanding how genetic variants impact this causal chain is essential. Although 2% of the population over age 65 are clinically diagnosed with Parkinson's disease, the defining pathology of disease (alpha-synuclein Lewy bodies) is discovered in 20% of brains from
population-based autopsy studies. We are therefore investigating the impact of genomic variation on directly measured Lewy pathology, neuronal loss in the midbrain substantia nigra, and progressive motor impairment, leveraging human subject cohorts with detailed clinical and pathological data. We also participate in collaborative studies for the functional genetic dissection of Alzheimer's disease, focusing on the responsible neuropathology, amyloid neuritic plaques and Tau neurofibrillary tangles.
population-based autopsy studies. We are therefore investigating the impact of genomic variation on directly measured Lewy pathology, neuronal loss in the midbrain substantia nigra, and progressive motor impairment, leveraging human subject cohorts with detailed clinical and pathological data. We also participate in collaborative studies for the functional genetic dissection of Alzheimer's disease, focusing on the responsible neuropathology, amyloid neuritic plaques and Tau neurofibrillary tangles.
Despite the promise of current human genetic methods, such as genome-wide association studies, they often fail to identify disease susceptibility genes with certainty, instead highlighting broad genomic regions. We are taking advantage of the rapid and powerful genetics available in the fruit fly Drosophila melanogaster in order to accelerate the validation of responsible genes and an understanding of their functions in disease pathogenesis. Expression of human amyloid-beta, Tau, or alpha-synuclein proteins in the fly nervous system recapitulates many core features of Alzheimer's disease and Parkinson's disease pathogenesis. We are testing candidate human susceptibility genes for functional genetic interactions in these fly models of neurodegeneration. Implicated molecular pathways are probed in greater depth, using both Drosophila and human genetic approaches. Our strategy has recently identified cell adhesion converging on the cytoskeleton as likely important for Tau-mediated neurodegeneration and Alzheimer's disease susceptibility, and we are now following up these insights to elucidate the detailed mechanisms.
Chronic traumatic encephalopathy (CTE) is the term coined for the neurodegenerative disease often suspected in athletes with histories of repeated concussion and progressive dementia. Histologically, CTE is defined as a tauopathy with a distribution of tau-positive neurofibrillary tangles (NFTs) that is distinct from other tauopathies, and usually shows an absence of beta-amyloid deposits, in contrast to Alzheimer's disease (AD). Although the connection between repeated concussions and CTE-type neurodegeneration has been recently proposed, this causal relationship has not yet been firmly established. Also, the prevalence of CTE among athletes with multiple concussions is unknown.
All participants had progressive neurocognitive decline prior to death; however, only 3 cases had post-mortem neuropathological findings consistent with CTE. The other 3 participants had pathological diagnoses
Parents can look for in their kids disease called Neuroblastoma. 8% of 30 Million Uninsured has Familial Cancer 1% of the 8% Kids has the ALK Gene on Chromosome2 that results in Neuroblastoma Cancer. Sam Houston Biotech Analytics Business Intelligence CIO Reports - 50% of the Moms with the Gene MYCN or CD44 Kids will have Neuroblastoma Cancer. The way Moms can recognized Neuroblastoma is a Abdominal Mass. The symptoms in high-risk patients are due to this tumor mass or bone pain from the cancer metastases. Extensive bone marrow metastasis may result in pancytopenia. Abdominal distention with respiratory compromise due to massive liver metastases may occur in infants. Because they originate in paraspinal ganglia, neuroblastomas may invade through neural foramina and compress the spinal cord extradurally, causing paralysis. The survival rate is twice as high if diagnosed in infants less that one years old. Genes that encode RNA-binding proteins (RBPs) such as PTB, hnRNP L, and SRSF1 are auto regulated to maintain a constant level of mRNA (Buratti and Baralle 2011).
This autoregulatory process may be achieved in part by selective alternative splicing events that trigger nonsense-mediated decay (NMD)-mediated RNA degradation (Lejeune and Maquat 2005). The general term
RUST (regulated unproductive splicing and translation) has been proposed to describe this category of gene regulation (Lareau et al. 2007a). Conrad also says that science labs use Genomics to generated multiple antibodies specific to phosphorylated TDP-43 by immunizing phosphopeptides of TDP-43, and analyzed
This autoregulatory process may be achieved in part by selective alternative splicing events that trigger nonsense-mediated decay (NMD)-mediated RNA degradation (Lejeune and Maquat 2005). The general term
RUST (regulated unproductive splicing and translation) has been proposed to describe this category of gene regulation (Lareau et al. 2007a). Conrad also says that science labs use Genomics to generated multiple antibodies specific to phosphorylated TDP-43 by immunizing phosphopeptides of TDP-43, and analyzed
FTLD-U and ALS brains by immunohistochemistry, immunoelectron microscopy, and immunoblots. In addition, we performed investigations 
aimed at identifying the responsible kinases, and we assessed the effects of phosphorylation on TDP-43 oligomerization and fibrillization.
aimed at identifying the responsible kinases, and we assessed the effects of phosphorylation on TDP-43 oligomerization and fibrillization.
As we see in the above picture of A Future National Football League (NFL ) Quarter Back Greyson Dean Secades Of Pope John XXIII High School In Houston, Texas playing is his State Championship Game and planning on being a "Pre-Med-Major" will have the benefit of having a Genomic Science Test to ensure that player thirty years from now will remain healthy after their Football playing days are over.
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