Stem Cell Treatments for Cerebral Palsy are Currently Available at ASCI
Because Cerebral Palsy is a condition that encompasses a group of non-progressive, non-contagious motor conditions that cause physical disability in human development, we aim to treat it with Stem Cell Therapy.
Cerebral refers to the cerebrum, which is the affected area of the brain (although the disorder most likely involves connections between the cortex and other parts of the brain such as the cerebellum), and palsy refers to disorder of movement. Cerebral palsy is caused by damage to the motor control centers of the developing brain and can occur during pregnancy, during childbirth or after birth up to about age three. Resulting limits in movement and posture cause activity limitation and are often accompanied by disturbances of sensation, depth perception and other sight-based perceptual problems, communication ability; impairments can also be found in cognition, and epilepsy is found in about one-third of cases. CP, no matter what the type, is often accompanied by secondary musculoskeletal problems that arise as a result of the underlying etiology.
Asphyxia, Infections, and Inflammation during Intrauterine development seemed to be the causes.
There are 4 types:
- Spastic - 80% and most common; hypertonic and have what is essentially a neuromuscularmobility impairment (rather than hypotonia or paralysis) stemming from an upper motor neuron lesion in the brain as well as the corticospinal tract or the motor cortex. This damage impairs the ability of some nerve receptors in the spine to properly receive gamma amino butyric acid, leading to hypertonia in the muscles signaled by those damaged nerves.
- Ataxic - caused by damage to the cerebellum, and it is common for individuals to have difficulty with visual and/or auditory processing.
- Dyskinetic - is mixed muscle tone – both hypertonia and hypotonia mixed with involuntary motions. People with Dyskinetic CP have trouble holding themselves in an upright, steady position for sitting or walking, and often show involuntary motions.
- Mixed - A combination of the above
Cerebral Palsy Stem Cell Treatment and stem cell therapy. Cerebral Palsy treatment studies and stem cell protocols:
A proteomic investigation into mechanisms underpinning corticosteroid effects on neural stem cells. Mol Cell Neurosci. 2017 Nov 08;: Authors: Al-Mayyahi RS, Sterio LD, Connolly JB, Adams CF, Al-Tumah WA, Sen J, Emes RD, Hart SR, Chari DM Abstract Corticosteroids (CSs) are widely used clinically, for example in pediatric respiratory distress syndrome, and immunosuppression to prevent rejection of stem cell transplant populations in neural cell therapy. However, such treatment can be associated with adverse effects such as impaired neurogenesis and myelination, and increased risk of cerebral palsy. There is increasing evidence that CSs can adversely influence key biological properties of neural stem cells (NSCs) but the molecular mechanisms underpinning such effects are largely unknown. This is an important issue to address given the key roles NSCs play during brain development and as transplant cells for regenerative neurology. Here, we describe the use of label-free quantitative proteomics in conjunction with histological analyses to study CS effects on NSCs at the cellular and molecular levels, following treatment with methylprednisolone (MPRED). Immunocytochemical staining showed that both parent NSCs and newly generated daughter cells expressed the glucocorticoid receptor, with nuclear localisation of the receptor induced by MPRED treatment. MPRED markedly decreased NSC proliferation and neuronal differentiation while accelerating the maturation of oligodendrocytes, without concomitant effects on cell viability and apoptosis. Parallel proteomic analysis revealed that MPRED induced downregulation of growth associated protein 43 and matrix metallopeptidase 16 with upregulation of the cytochrome P450 family 51 subfamily A member 1. Our findings support the hypothesis that some neurological deficits associated with CS use may be mediated via effects on NSCs, and highlight putative target mechanisms underpinning such effects. PMID: 29128319 [PubMed - as supplied by publisher]Read more...