Alternative Strategy for Alzheimer’s Disease: Stress Response Triggers

Sonneborn, Joan Smith

doi:10.1155/2012/684283

Cited by 7 publications

(9 citation statements)

References 65 publications

(78 reference statements)

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“…Strenuous exercise disturbs the antioxidant equilibrium by increasing ROS levels. However, regular exercise upregulates endogenous antioxidant levels and reduces oxidative damage (34). As continued exposure to uncontrolled oxidative stress is an initiator of various chronic diseases and cancer, cells have developed a range of antioxidant strategies, including enzymatic and non-enzymatic antioxidants (35).…”

Section: Ros Involvement In the Pathogenesis Of Fatty Liver Diseasementioning

confidence: 99%

Diet induces hepatocyte protection in fatty liver disease via modulation of PTEN signaling (Review)

et al. 2020

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Fatty liver disease (FLD) is characterized by accumulation of excess fat in the liver. The underlying molecular mechanism associated with the progression of the disease has been in elusive. Hepatocellular demise due to increased oxidative stress resulting in an inflammatory response may be a key feature in FLD. Recent advances in molecular biology have led to an improved understanding of the molecular pathogenesis, suggesting a critical association between the PI3K/AKT/PTEN signaling pathway and FLD. In particular, PTEN has been associated with regulating the pathogenesis of hepatocyte degeneration. Given the function of mitochondria in reactive oxygen species (ROS) generation and the initiation of oxidative stress, the mitochondrial antioxidant network is of interest. It is vital to balance the activity of intracellular key molecules to maintain a healthy liver. Consequently, onset of FLD may be delayed using dietary protective agents that alter PTEN signaling and reduce ROS levels. The advancement of research on dietary regulation with a focus on modulatory roles in ROS generation and PTEN associated signaling is summarized in the current study, supporting further preventive and therapeutic exploration.

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Section: Ros Involvement In the Pathogenesis Of Fatty Liver Diseasementioning

confidence: 99%

Diet induces hepatocyte protection in fatty liver disease via modulation of PTEN signaling (Review)

et al. 2020

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“…In fact, inducing stress response has been proposed recently as a treatment method for AD (Smith Sonneborn, 2012). On the other hand, excessive thinking can be unhealthy.…”

Section: Increased Dna Damage In the Brain From Thinkingmentioning

confidence: 99%

“…Considering these beneficial effects from the initial DNA damage, it is tempting to suggest that periodic application of a small amount of oxidative damage to the brain would be beneficial to brain health. This method of using low level stressors to upregulate protection systems has recently been proposed as a method of reducing the impact of neurodegenerative diseases (Smith Sonneborn, 2012;Stranahan and Mattson, 2012).…”

Section: Low Dose Radiation Adaptive Response To Control Neurodegenermentioning

confidence: 99%

Low Dose Radiation Adaptive Protection to Control Neurodegenerative Diseases

Doss¹

2013

Dose-Response

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ᮀ Concerns have been expressed recently regarding the observed increased DNA damage from activities such as thinking and exercise. Such concerns have arisen from an incomplete accounting of the full effects of the increased oxidative damage. When the effects of the induced adaptive protective responses such as increased antioxidants and DNA repair enzymes are taken into consideration, there would be less endogenous DNA damage during the subsequent period of enhanced defenses, resulting in improved health from the thinking and exercise activities. Low dose radiation (LDR), which causes oxidative stress and increased DNA damage, upregulates adaptive protection systems that may decrease diseases in an analogous manner. Though there are ongoing debates regarding LDR's carcinogenicity, with two recent advisory committee reports coming to opposite conclusions, data published since the time of the reports have overwhelmingly ruled out its carcinogenicity, paving the way for consideration of its potential use for disease reduction. LDR adaptive protection is a promising approach to control neurodegenerative diseases, for which there are no methods of prevention or cure. Preparation of a compelling ethics case would pave the way for LDR clinical studies and progress in dealing with neurodegenerative diseases.

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“…Tolerance strategies and drugs employed to treat the common stresses are candidates to treat HIV. Mimetics of tolerance, and stress resistance agents used to tolerate stress in different organisms are reservoirs for drug intervention [1][2][3] applicable in HIV therapeutics.…”

Section: Introductionmentioning

confidence: 99%

Novel Anti-Retroviral Drug Targets: Interfering siRNA and Mitochondrial TERT Expression

Smith-Sonneborn

2016

Virol Mycol

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Telomerase can be touted as the miracle anti-aging enzyme that reverses the age-related attrition of telomere ends. The catalytic subunit of telomerase, TERT telomerase reverse transcriptase, is known to function as an RNA dependent DNA polymerase in the nucleus (TERT-TERC), as an RNA dependent RNA polymerase, an RdRP (TERT-RMRP), in mitochondria, and, as TERT alone interacting with master regulators for cell and organellar protection to promote global survival and rejuvenation potential. TERT shows conservation of the viral polymerase structure, and like viral polymerases, is capable of producing cDNA, double stranded RNA, and like HIV reverse transcriptase, is inhibited by some HIV reverse transcriptase inhibitors. TERT also shows promiscuous partnering with RNA elements, RMPR, tRNA, and TERC. TERT, with its versatile viral-like functions, seems like a valuable hostage for viral infection. Telomerase is inhibited by viral proteins. When the role of telomerase in HIV infection is reviewed, telomerase modulation emerges as a valuable player in HIV therapy intervention. Induced viral protein and some reverse transcriptase HIV drugs promote TERT deficit which might be counteracted by TERT up regulation, or preference for use of drugs that do not target host reverse transcriptase, in order to preserve the health promotion of TERT pathways especially mitochondrial protection against oxidative stress, and inhibition of pathways that promote immune deficiency. Telomerase "dark side" dysfunctional overexpression might be targeted using an anti-cancer-like vaccine, delivered selectively to viral reservoirs. The use of siRNA's to inactivate proteins that promote viral survival offer promising potential success in anti-retroviral therapy, with the ability to block mico RNAs favorable for viral progression. Strategies and therapy that interfere with the HIV-TAR interaction offer the desirable ability to stop infection before it starts. Mimetics of exercise, hibernation, anti-aging supplements, and mitochondrial targeted antioxidants offer antiviral potential and disease vulnerability from fallout of immune deficiency. SchramlE, Grillari J (2012) From cellular senescence to age-associated diseases: the miRNA connection. Longev Healthspan 1: 10. 76. Bai XY, Ma Y, Ding R, Fu B, Shi S, et al. (2011) miR-335 and miR-34a Promote renal senescence by suppressing mitochondrial antioxidative enzymes. J Am Soc Nephrol 22: 1252-1261. Citation: Smith-Sonneborn J (2016) Novel Anti-Retroviral Drug Targets: Interfering siRNA and Mitochondrial TERT Expression. Virol-mycol 5: 150.

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Alternative Strategy for Alzheimer’s Disease: Stress Response Triggers

Cited by 7 publications

References 65 publications

Diet induces hepatocyte protection in fatty liver disease via modulation of PTEN signaling (Review)

Diet induces hepatocyte protection in fatty liver disease via modulation of PTEN signaling (Review)

Low Dose Radiation Adaptive Protection to Control Neurodegenerative Diseases

Novel Anti-Retroviral Drug Targets: Interfering siRNA and Mitochondrial TERT Expression

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