Dementia Treatment

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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.




Integrated Health System'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.

IHS doctors are here to help you at every step in your journey to health. To schedule your 15 min or 30 min consultation with a doctor from Integrated Health Systems please click the link below.


  • Please note that the default length of an appointment is 15-min, so if you would like a 30-min appointment please select two simultaneous slots.

  • Please note that a 15-minute consultation with our doctor will cost you $100 USD, and a 30-minute consultation will cost you $200 USD. If you choose to receive a treatment from us we will deduct the cost of the appointment from your treatment costs.

  • Finally, once you have secured an appointment slot, or slots, we'll send you an invoice for the appropriate amount. Please pay this invoice within 24 hours of reception. otherwise your appointment will be cancelled.




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.



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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

Our technology and care, your healthy longevity:

IHS, in partnership with BioViva, is dedicated to provide you with the latest breakthroughs in medical technologies to help you at this difficult time in your life. Together we will tackle your cancer head-on and we are confidently hopeful for successful outcome.