A Novel Gene Therapy To Treat One Of The World’s Biggest Growing Chronic Disease: Dementia and Alzhiemer’s17 July 2018
Research studies indicate that telomerase gene therapy may not only reverse Alzheimer’s Disease and other dementias, but it may even protect people from developing such diseases.
This is indeed hopeful news for the nearly 50 million victims of Alzheimer’s or related dementia worldwide as well as for the millions of aging people with Parkinson’s and aging-related mental decline.
Telomerase gene therapy appears to rejuvenate microglial (the immune cells of the brain) cells in Alzheimer’s Disease according to promising research study data.
HOW IT WORKS:
Neurons (nerve cells) are the primary components of the central nervous system (CNS). Neurons connect to each other to form neural networks, and communicate via electrical and chemical signals at specialized connections called synapses. There are over 100 trillion synapses in the human brain.
The brain is about 10% neurons and 90% neural network support cells, called neuroglia, or glial cells, which surround and insulate neurons, protect them from damage, and supply them with nutrients and oxygen. Neuroglia are often found to malfunction in neurological disorders such as Alzheimer’s Disease or amyotrophic lateral sclerosis (ALS).
Telomerase is an enzyme that protects the ends of chromosomes, called
telomeres, which are otherwise shortened each time cells divide. In adults, most cells in the body no longer express telomerase, and so their chromosomes become shorter and cells age (become senescent).
Telomerase gene therapy appears to rejuvenate a subtype of glial cells, called microglia, which act as the first and main form of active immune defense in the central nervous system (CNS). These cells mediate immune responses in the central nervous system by clearing toxins, microbes, cellular debris and dead neurons from nervous tissue through a process called phagocytosis (cell eating). They also help in the formation and pruning of synapses.
In addition, there is mounting evidence to indicate that telomerase plays an active role in protection from Tau pathology, an accumulation of malfunctioning protein aggregates (plaques) seen Alzheimer’s disease.
Integrated Health System’s gene therapy targeting neurodegeneration utilizes an adeno-associated virus (AAV) vector platform, modified for the enhanced telomerase gene therapy 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.
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Meet our doctor: Dr. Jason Williams, MD
Dr Williams CMO is a radiologist. He obtained his medical degree from Louisiana State University and has also completed an internship in Internal Medicine at The University of South Alabama. He is passionate about gene and cellular therapies, administered under image guidance. Image guided cancer therapies are also one of his interests. For several years, he did research with adenoviral vector technology used to treat cancer. He was selected for the RSNA Research Fellow Award. He has completed training in image guided cancer and spine procedures, and is board certified by the American Board of Radiology. He has research interests in gene therapy and stem cell reprogramming, as well as using CT and MRI for minimally invasive procedures related to the spine and cancer.
Evidence for telomerase therapy for Alzheimer’s
We intend to test telomerase gene therapy to rejuvenate microglial cells in our Alzheimer’s Disease trial, building on promising research study data.
The pre-clinical and biomedical data for our study has been reviewed from the following studies:
- 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