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Author Topic: Parkinsons neuron degeneration halted in mice  (Read 223 times)

morganism

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Parkinsons neuron degeneration halted in mice
« on: July 02, 2020, 12:22:00 AM »
Reversing a model of Parkinson’s disease with in situ converted nigral neurons

https://www.nature.com/articles/s41586-020-2388-4

One-time treatment generates new neurons, eliminates Parkinson's disease in mice

https://www.sciencedaily.com/releases/2020/06/200625102540.htm

"Researchers have discovered that a single treatment to inhibit a gene called PTB in mice converts native astrocytes, brain support cells, into neurons that produce the neurotransmitter dopamine. As a result, the mice's Parkinson's disease symptoms disappear. "

"The treatment works like this: The researchers developed a noninfectious virus that carries an antisense oligonucleotide sequence -- an artificial piece of DNA designed to specifically bind the RNA coding for PTB, thus degrading it, preventing it from being translated into a functional protein and stimulating neuron development.

Antisense oligonucleotides, also known as designer DNA drugs, are a proven approach for neurodegenerative and neuromuscular diseases "


morganism

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Re: Parkinsons neuron degeneration halted in mice
« Reply #1 on: November 21, 2020, 02:53:22 AM »
an aging article on hyperbaric effect on telomere length, and t cells

Hyperbaric oxygen therapy increases telomere length and decreases immunosenescence in isolated blood cells : a prospective trial

https://www.aging-us.com/article/202188/text

" These intermittent hyperoxic exposures induce an adaptive response which includes increased upregulation of antioxidants genes [32] and production of antioxidants/scavengers that adjust to the increased ROS generation causing the ROS/scavenger ratio to gradually becomes similar to the ratio under a normal oxygen environment. However, because the scavenger elimination half-life (T1/2) is significantly longer than the T1/2 of ROS, upon return to normoxia, following repeated hyperoxic exposures, there are significantly higher levels of scavengers and increased antioxidant activity [13, 18]. Thus, similar to physical exercise and caloric restriction, a daily repeated HBOT protocol can induce the hormesis phenomenon. Single exposures increase ROS generation acutely, triggering the antioxidant response, and with repeated exposures, the response becomes protective [13, 18].

Additionally, intermittent hyperoxic exposures induce many of the physiological responses that occur during hypoxia [13]. HBOT induces the release of transcription factors called hypoxic induced factors (HIF) and increase their stability and activity [14]. In turn, HIF induces a cellular cascade including vascular endothelial growth factor and angiogenesis induction, mitochondria biogenesis, stem cells mobilization and SIRT1 increased activity [18]. Our study confirms increased HIF expression is induced by repetitive HBOT exposures, which gradually decreases towards normalization of HIF levels at nonmonic environment."