Is anything more quintessential of aging as sensory loss of hearing (and vision?)
Here age related decline in Nrf2 expression (lack of bullets) leads to cortical auditory degeneration.
Step 1. More antioxidant enzyme bullets. Step 2. Increase Vagal tone, calm down microglia. Step 3. BrainHQ.com to increase BDNF and rebuild a parallel processing auditory cortex.
This is something I literally did in a study N of 1.
This statistically valid research of step 3 alone produces a 135% increase in auditory processing speed and 230% increase in visual processing speed.
Why is the processing speed so important?. The sharp area of central focal vision is small, like a flashlight beam, that uses scanning and processing to see the bigger picture. PROCESSING, important for seeing, hearing, comprehending and remembering. Auditory sampling speed determines processing speed and accuracy.
Bullets, Vagal tone and BDNF build. Age related Epigenetic switching off of Nrf2, alpha 7 Nicotinic acetylcholine receptors and BDNF CpG gene promoter sites is directly correlated to aging and disease in cells, tissues, organs and people.
Age-associated decline in Nrf2 signaling and associated mtDNA damage may be involved in the degeneration of the auditory cortex: Implications for central presbycusis.
Central presbycusis is the most common sensory disorder in the elderly population, however, the underlying molecular mechanism remains unclear. NF‑E2‑related factor 2 (Nrf2) is a key transcription factor in the cellular response to oxidative stress, however, the role of Nrf2 in central presbycusis remains to be elucidated. The aim of the present study was to investigate the pathogenesis of central presbycusis using a mimetic aging model induced by D‑galactose (D‑gal) in vivo and in vitro. The degeneration of the cell was determined with transmission electron microscopy, terminal deoxynucleotidyl transferase‑mediated deoxyuridine 5'‑triphosphate nick‑end labeling staining, and senescence‑associated β‑galactosidase staining. The expression of protein was detected by western blotting and immunofluorescence. The quantification of the mitochondrial DNA (mtDNA) 4,834‑base pair (bp) deletion and mRNA was detected by TaqMan quantitative polymerase chain reaction (qPCR) and reverse transcription‑qPCR respectively. Cell apoptosis and intracellular ROS in vitro were determined with flow cytometry. The levels of nuclear Nrf2, and the mRNA levels of Nrf2‑regulated antioxidant genes, were downregulated in the auditory cortex of aging rats, which was accompanied by an increase in 8‑hydroxy‑2'‑deoxyguanosine formation, an accumulation of mtDNA 4,834‑bp deletion, and neuron degeneration. In addition, oltipraz, a typical Nrf2 activator, was found to protect cells against D‑gal‑induced mtDNA damage and mitochondrial dysfunction by activating Nrf2 target genes in vitro. It was also observed that activating Nrf2 with oltipraz inhibited cell apoptosis and delayed senescence. Taken together, the data of the present study suggested that the age‑associated decline in Nrf2 signaling activity and the associated mtDNA damage in the auditory cortex may be implicated in the degeneration of the auditory cortex. Therefore, the restoration of Nrf2 signaling activity may represent a potential therapeutic strategy for central presbycusis.
Joseph Thomas (Tony) Liverma
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