stemcell-treatment-ALS-neural-cells

Neurogenic Treatment of ALS w/ MSC+ Stem Cells

UPDATED August 03, 2020 – ALS (short for Amyotrophic Lateral Sclerosis) is a progressive neurodegenerative disease of the upper & lower motor neurons in the brainstem, motor cortex, and spinal cord. Clinical trials and previous research in medical journals have shown that the typical life expectancy after diagnosis is three to approximately six years. The actual cause of ALS and Motor Neuron Disease varies from patient to patient; however, it’s widely believed that the underlying issue for a majority of patients can be traced to the dysfunction or misregulation of a vital neuroprotein known as TDP-43.[1]

Amyotrophic lateral sclerosis (ALS), motor neurone disease (MND)

Motor neuron diseases (MND) are a family of conditions and include primary lateral sclerosis (PLS), amyotrophic lateral sclerosis (ALS), progressive muscular atrophy (PMA), monomelic amyotrophy (MMA), pseudobulbar palsy and progressive bulbar palsy.

Diagnosing ALS

The diagnosis and classification of MND to ALS occurs depending on how fast the patient’s disease progresses through stages and if the condition is considered inherited/familial or sporadic/idiopathic. For most patients, symptoms of ALS are first experienced in the face or throat muscles. This early stage (onset) stage occurs when the lower motor neurons and motor neurons and neurotransmitters in the brain stem (bulb/medulla oblongata) start to die. This early form of ALS is classified as “onset bulbar ALS.” Over time the disease spreads to other areas, including the spinal cord motor neurons.

ALS vs. PLS, and PMA

Classic symptoms of ALS occur in about 65% of all cases and affect both the upper and lower motor neurons. Classical ALS can be classified as bulbar-onset or spinal-onset (limb-onset) ALS disease. The classification of ALS is unique as the diagnosis of PLS (Primary lateral sclerosis) affects only the upper motor neurons in the arms and legs while PMA (progressive muscular atrophy) affects the lower motor neurons only. Other variations of ALS include Respiratory-onset ALS, fail leg syndrome (leg amyotrophic diplegia,) flail arm syndrome (brachial amyotrophic diplegia) and isolated bulbar ALS. Current clinical applications offer a better prognosis for Primary lateral sclerosis than classic ALS due to its slower rate of progress, which results in less functional decline. Males are more likely to develop young-onset ALS while juvenile ALS is much more likely to be heredity in nature than adult-onset ALS.

ALS or Lou Gehrig’s disease is a very aggressive neurological-degenerative disease that impacts the nerve cells within the brain and the spinal cord. In particular, ALS refers to the degeneration of the motor neurons that reach out from the brain towards the spinal cord and then towards the muscles. ALS will cause the motor neurons, cell signaling and neurotransmitters to eventually die and with it, the capability of the brain to instigate and manage the voluntary muscle movements similar to Parkinson’s Disease and MS. This will eventually result in total paralyzation for the patient during the late stage of the illness.[2]

Signs and Symptoms of ALS

Due to the rapid degeneration of the upper and lower motor neurons, Neurodegenerative diseases such as ALS usually cause muscle atrophy, neuropathic pain, muscle spasticity, frequent muscle cramps, or spasms throughout the body. The symptoms are often mistaken for other conditions such as peripheral neuropathy and over time patients with ALS lose the ability to control voluntary movements, bowel function and the use of extraocular muscles that are responsible for the movement of the eyes. ALS isn’t considered to be an example of autoimmune disease, although some medical researchers believe that it may be, partly due to a seemingly disorganized immune response.

Along with physical degeneration, patients with ALS also suffer from behavioral or cognitive dysfunctions, which often get misdiagnosed as frontotemporal dementia. Some common symptoms include Repeat gestures or phrases, loss of inhibition, apathy, language problems, and verbal memory loss. About 50% of patients with bulbar-onset ALS experience depression and extreme emotional states where they laugh or cry for no apparent reason. Nociceptive pain is another common symptom as patients report frequent muscle contractions in the cervical spine ( neck area), lower back pain, shoulder pain, or pressure in the stomach area.

Causes & Risk factors of ALS

Despite rapid progress in understanding the sides, the cause of ALS is relatively unknown but are generally attributed has hereditary (familial) or sporadic (environmental.) With advancements in molecular diagnostics, the genetic factors associated with ALS are better understood and more straightforward to diagnose than environmental factors. There is no single specific cause of environmental ALS, but research has proven that the neurodegenerative damage associated with ALS accumulates over long periods.

Chances of Getting ALS

Scientific studies have shown that familial (hereditary) ALS accounts for less than 10% of all confirmed cases. Inherited ALS is either an X-linked dominant pattern or autosomal recessive pattern. Each parent carries one copy of the mutated gene, but often do not show any signs or symptoms of the condition. For this reason, autosomal recessive ALS is often misdiagnosed as environmental (sporadic) ALS. The most common markers for heredity ALS are C9orf72, SOD1, FUS, and TARDBP but there are over 20 genes that are linked to familial ALS and the only way to accurately identify genetic mutations are with DNA screenings.

Genetic Testing for ALS

Since DNA testing was not prevalent in previous generations, it’s often difficult to predict unless proactively screened for. Clinical diagnosis for ALS typically requires mutations in at least 2 (or more) genes due to oligogenic inheritance. The regeneration center does not offer gene therapies for ALS but can provide DNA sequencing tests for 20 most common genetic causes of familial Amyotrophic Lateral Sclerosis  including: ALS2, TBK1, SOD1, DCTN1, SPG11, TARDBP, KIF5A, FUS, OPTN, PFN1, SETX, CHCHD10, CHMP2B, MATR3, UBQLN2, VAPB, TFG, VCP, SIGMAR1 and SQSTM1.

Sporadic vs. Isolated ALSLou Gehrig's disease

Patients  with sporadic ALS account for over 90% of all cases. It’s important to note that the symptoms for familial and sporadic ALS are nearly identical and can only be differentiated genetically. For patients with no known family history and mutated genes, environmental factors are typically the cause. ALS researchers have identified various factors, such as exposure to heavy metals and environmental toxins like lead, chemical exposure, pesticides, serum uric acid, DDT, organochlorine, dieldrin, and toxaphene.

Evidence is often inconclusive, but some potential environmental factors might include:

  • Physical trauma due to accident
  • Repeat head injuries due to sports like boxing, MMA, NFL, and other contact sports
  • Electromagnetic field exposure
  • Severe traumatic brain injury often misdiagnosed as chronic traumatic encephalopathy (CTE) or ataxia

ALS progression rates vary from person to person, but common symptoms include:

Stem-Cell-Treatment-ALS

  • Stiff finger joints
  • Uneven fine motor skills
  • Weakness in hands due to muscle atrophy
  • Problems with keeping head up
  • Problems keeping good posture
  • Weak muscles in feet, ankle or legs
  • Benign fasciculation syndrome (BFS)
  • Sensory neuropathy
  • Slurring of words during speech or trouble swallowing
  • Frequent muscle cramps
  • Random twitching of tongue, arms or shoulders
  • The trouble with the respiratory system and breathing normally

Stem Cell Therapy for ALS

The Regeneration Center offers a very safe and effective functional medical treatment plans for complex neurodegenerative conditions such as MND & ALS along with other treatments for Brain Injuries, strokes and Alzheimer’s all essentially focuses on stopping the spread and potential reduction of symptoms related to the illness. Neuro Stem cells and exosomes seek to slow down and reverse the consequences of ALS and restore the quality of life for the patient.[3]

PRECAUTIONS & RISKS
Stem Cells for treating degenerative neurological conditions such as ALS are not appropriate or effective for all cases. Patients with late stage diagnosis, Unidentifiable Idiopathic diagnosis, history of cardiovascular disease – heart attacks or travel restrictions may not qualify for clinical program or support services.

Caring for ALS Patients

The Regeneration institute policy prohibits the use of embryonic stem cells or stem cells derived from animals, ie, “Live Cells.” The enhanced neural stem cells and nerve growth factors are isolated and expanded into the required quantities and lineages including glial restricted progenitors cells (GRP), oligodendrocyte progenitor cells (OPCs), astrocytes, and neurons.

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 Cell Expansion with Neural Growth Factors

After collection, the stem cells are concentrated then isolated to measure the overall quantity and quality of the collected stem cells. Only certain types of activated neural progenitor stem cells can transform into the necessary types of cells. These activated stem cells are capable of regenerating damaged tissues such as the myelin sheath needed in clinical therapies for ALS and spinal muscular atrophy.[4]

Cell Infusion Stage

The day after the expansion of the enriched Mesenchymal stem cells (MSC+) and neural progenitor cells can be implanted into the patient through basically one of two methods. IV Drip or direct injection. For severe cases or patients with idiopathic conditions, direct lumbar injections may be required. For cases requiring direct injections into the spinal vertebra (in between L4 and L5) under local anesthesia. The patients are advised to stay to get a couple of hours within the recovery space following the direct injection.

Management of ALS with Stem Cells


Number of  Stages in Clinical Program: Multi-stage process using multi-combination infusions of glial restricted progenitors cells (GRP), oligodendrocyte progenitor cells (OPCs), astrocytes, and neurons per Phase. The types of cells infusions may include Enhanced Neural Stem cells from Differentiated Cell Lineages via IV Drip, Intrathecal, and lumbar puncture per the patient’s needs.

Physical Rehabilitation: Physical Rehab after completion of therapy is advised. Physical rehabilitation post-therapy and can be provided upon request for 2-4 hours per day and up to 5 days per week. 
Medical visas and extended stay accommodations at a hotel or furnished apartments for the patient and family can also be included upon request.

ALS Treatment Guidelines

For qualifying patients, the therapy will require a minimum of 2-3 weeks in total. Due to the significant differences and stages of damage, our medical team will need to review the potential candidate’s medical records and eligibility for treatment and travel to Thailand. Upon approval, a clinical plan will be provided that will include the specifics of the therapy that will include: total number nights required along with the total medical related costs and stem cell transplant fees (excluding accommodations or flights). To begin the qualification process for the multi-stage ALS stem cell therapy,  please prepare your recent medical records such as list of current medications (radicut/radicava, edaravone, riluzole) Brain MRI’s, CT Scans, or PET Scans (Preferred) and contact us today.

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Published Clinical Citations

  • [1] ^ Kwon, Min-Soo, Min-Young Noh, Ki-Wook Oh, Kyung-Ah Cho, Byung-Yong Kang, Kyung-Suk Kim, Young-Seo Kim, and Seung H Kim. 2014. The immunomodulatory effects of human mesenchymal stem cells on peripheral blood mononuclear cells in ALS patients. Journal of neurochemistry, no. 2 (July 31). doi:10.1111/jnc.12814. https://www.ncbi.nlm.nih.gov/pubmed/24995608

  • [2] ^ Mazzini, Letizia, Angelo Vescovi, Roberto Cantello, Maurizio Gelati, and Alessandro Vercelli. 2016. Stem cells therapy for ALS. Expert opinion on biological therapy, no. 2 (January 9). doi:10.1517/14712598.2016.1116516. https://www.ncbi.nlm.nih.gov/pubmed/26558293

  • [3] ^ Poungvarin, N, and A Viriyavejakul. 1991. Motor neurone disease in Thailand: the clinical aspects of 77 patients. Journal of the Medical Association of Thailand = Chotmaihet thangphaet, no. 4. https://www.ncbi.nlm.nih.gov/pubmed/1940701

  • [4] ^ Thomsen, Gretchen M, Genevieve Gowing, Soshana Svendsen, and Clive N Svendsen. 2014. The past, present and future of stem cell clinical trials for ALS. Experimental neurology (March 6). doi:10.1016/j.expneurol.2014.02.021. https://www.ncbi.nlm.nih.gov/pubmed/24613827