I’m a Doctor

We intend to test telomerase gene therapy to rejuvenate microglial cells in a Alzheimer’s Disease trial, building on promising research study data.

There is mounting evidence to indicate telomerase plays an active role in protection from Tau Pathology and various experiments have encouraged us to pursue this therapy with the goal of eliminating the suffering this disease brings.

telomerase

A RESEARCH REVIEW: Neurodegeneration and Telomerase

1. Critically short telomeres lead to oxidative stress and neuroinflammation – established contributors to Alzheimer’s pathology.
2. The TERT protein appears to reduce toxic Tau tangle accumulation and alleviate mitochondrial stress.
3. Senescent microglial cells are linked to Alzheimer’s. Telomerase extension can prevent cellular senescence by repairing critically short telomeres.
4. Aggregated amyloid beta and Alzheimer’s pathology inhibit telomerase expression; accelerating disease progression by accelerating microglial senescence.
5. Immune cell senescence is associated with Alzheimer’s onset.
6. Astrocyte senescence is also correlated with Alzheimer’s onset, and may be prevented by telomerase induction.
7. Old microglia exposed to the conditioned media of young microglia are better able to reduce amyloid plaque formation.

Our Therapy

BioViva’s gene therapy targeting neurodegeneration utilizes an adeno-associated virus (AAV) vector platform modified for the enhanced delivery to neural tissue. The genes to treat the disorder are inserted into the virus, which then delivers the genes of interest to the patient’s cells. In recent years AAV gene therapies have been tested in humans with great success and no evidence of adverse effects. There are numerous clinical trials currently being conducted with AAV gene therapy for many diseases.

Our AAV telomerase gene therapy is delivered via intrathecal injection into the cerebrospinal fluid, enabling neural delivery.

Who is Dr. Jason Williams?

Dr. Jason Williams has been delivering gene therapy to patients for over 14 years. Furthermore, he was one of the first doctors to deliver P53 gene therapy to cancer patients in North America. Over the past decade, a number of new cancer therapies have been developed. Such as:

  • Gene therapy
  • Tumour ablation
  • Immunotherapy

Continual refinement, updating & perfection is required of these treatments. Offering the best long term outcomes, and the highest level of care to patients. At Integrated Health Systems, our primary concern is your health and wellbeing. We understand that this period of your life can be testing. We only deliver the very best level of care, and aim to fight your cancer completely. We wish you a long and healthy future and look forward to working with you.

References

Agostinho, Paula, Rodrigo A Cunha, and Catarina Oliveira. “Neuroinflammation, oxidative stress and the pathogenesis of Alzheimer’s disease.” Current pharmaceutical design 16.25 (2010): 2766-2778

Bhat, Rekha, et al. “Astrocyte senescence as a component of Alzheimer’s disease.” PloS one 7.9 (2012): e45069

Chinta, Shankar J., et al. “Cellular senescence and the aging brain.” Experimental gerontology 68 (2015): 3-7

Daria et al. “Young microglia restore amyloid plaque clearance of aged microglia”. The EMBO Journal. (2016)

Flanary, Barry E., et al. “Evidence that aging and amyloid promote microglial cell senescence.” Rejuvenation research 10.1 (2007): 61-74

Haendeler, Judith, et al. “Mitochondrial telomerase reverse transcriptase binds to and protects mitochondrial DNA and function from damage.” Arteriosclerosis, thrombosis, and vascular biology 29.6 (2009): 929-935

Kronenberg, Golo, et al. “Repression of telomere-associated genes by microglia activation in neuropsychiatric disease.” European Archives of Psychiatry and Clinical Neuroscience (2016): 1-5.

Maccioni, Ricardo B., et al. “The role of neuroimmunomodulation in Alzheimer’s disease.” Annals of the New York Academy of Sciences 1153.1 (2009): 240-246

Mhatre, Molina, Robert A. Floyd, and Kenneth Hensley. “Oxidative stress and neuroinflammation in Alzheimer’s disease and amyotrophic lateral sclerosis: common links and potential therapeutic targets.” Journal of Alzheimer’s disease 6.2 (2004): 147-157

Panossian, L. A., et al. “Telomere shortening in T cells correlates with Alzheimer’s disease status.” Neurobiology of aging 24.1 (2003): 77-84.

Rolyan, Harshvardhan, et al. “Telomere shortening reduces Alzheimer’s disease amyloid pathology in mice.” Brain (2011)

Salminen, Antero, et al. “Astrocytes in the aging brain express characteristics of senescence‐associated secretory phenotype.” European Journal of Neuroscience 34.1 (2011): 3-11

Silva, Patricia Natalia Oliveira, et al. “Promoter methylation analysis of SIRT3, SMARCA5, HTERT and CDH1 genes in aging and Alzheimer’s disease.” Journal of Alzheimer’s Disease 13.2 (2008): 173-176

Spilsbury, Alison, et al. “The role of telomerase protein TERT in Alzheimer’s disease and in tau-related pathology in vitro.” The Journal of Neuroscience 35.4 (2015): 1659-1674

Wang, Jiasi, et al. “New insights in amyloid beta interactions with human telomerase.” Journal of the American Chemical Society 137.3 (2015): 1213-1219

Zhu, Haiyan, Weiming Fu, and Mark P. Mattson. “The Catalytic Subunit of Telomerase Protects Neurons Against Amyloid β‐Peptide‐Induced Apoptosis.” Journal of neurochemistry 75.1 (2000): 117-124

Zhu, Xiongwei, et al. “Activation of p38 kinase links tau phosphorylation, oxidative stress, and cell cycle-related events in Alzheimer disease.” Journal of Neuropathology & Experimental Neurology 59.10 (2000): 880-888

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