Nicotine and cigarette smoke modulate Nrf2-BDNF-dopaminergic signal and neurobehavioral disorders in adult rat cerebral cortex<sup>#</sup>

Naha, Nibedita; Gandhi, Darshan; Ak, Güntülü; Prakash, Jamalpur Ravi

doi:10.1177/0960327117698543

Cited by 16 publications

(13 citation statements)

References 76 publications

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“…However, there were several limitations in this study. First, previous studies reported that exercise [ 42 ], smoking [ 43 ] and alcohol [ 44 ] were correlated with cognition. However, unfortunately, we did not collect the data for exercise level, smoking or alcohol drinking in our current study, which will be remedied in future investigation.…”

Section: Discussionmentioning

confidence: 99%

Cognition, serum BDNF levels, and BDNF Val66Met polymorphism in type 2 diabetes patients and healthy controls

et al. 2017

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Background and aimsType 2 diabetes (T2DM) is associated with cognitive deficits. However, their pathophysiological mechanisms are still unknown. Recent study suggests that brain-derived neurotrophic factor (BDNF) is correlated with cognitive deficits in T2DM patients. This study was to determine whether altered serum BDNF levels and cognitive deficits depended on the BDNF Val66Met polymorphism in T2DM.ResultsThe BDNF Val66Met polymorphism may not contribute directly to the susceptibility to T2DM. The total and nearly all index scores (all p < 0.01) except for the attention and visuospatial/constructional indexes (both p > 0.05) of RBANS were markedly decreased in T2DM compared with healthy controls. Serum BDNF levels were significantly lower in patients than that in controls (p < 0.001), and BDNF was positively associated with delayed memory in patients (p < 0.05). The Met variant was associated with worse delayed memory performance among T2DM patients but not among normal controls. Moreover, serum BDNF was positively associated with delayed memory among Met homozygote patients (β = 0.29, t = 2.21, p = 0.033), while serum BDNF was negatively associated the RBANS total score (β = –0.92, t = –3.40, p = 0.002) and language index (β = −1.17, t = –3.54, p = 0.001) among Val homozygote T2DM patients.ConclusionsBDNF gene Val66Met variation may be associated with cognitive deficits in T2DM, especially with delayed memory. The association between lower BDNF serum levels and cognitive impairment in T2DM is dependent on the BDNF Val66Met polymorphism.MethodsWe recruited 311 T2DM patients and 346 healthy controls and compared them on the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS), serum BDNF levels, and the BDNF Val66Met polymorphism.

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Section: Discussionmentioning

confidence: 99%

Cognition, serum BDNF levels, and BDNF Val66Met polymorphism in type 2 diabetes patients and healthy controls

et al. 2017

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“…Conversely, tobacco smoking cessation reduces risk for developing AD/ADRD (Choi et al, 2018). Tobacco smoke is a potent oxidative stressor (Pryor and Stone, 1993) that induces systemic oxidative stress (Sandhya et al, 2016) and depletes Nrf2 expression (Naha et al, 2018). Smoking-induced oxidative stress has been demonstrated in humans by quantifying a CSF biomarker, F2-isoprostane (iPF2α-III), levels of which are elevated in both cognitively normal elderly smokers and in probable AD smokers (Durazzo et al, 2014b(Durazzo et al, , 2016a.…”

Section: Tobacco Use Disordermentioning

confidence: 99%

Supraphysiologic-dose anabolic–androgenic steroid use: A risk factor for dementia?

Kaufman

Kanayama

Hudson

et al. 2019

Neuroscience & Biobehavioral Reviews

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Supraphysiologic-dose anabolic-androgenic steroid (AAS) use is associated with physiologic, cognitive, and brain abnormalities similar to those found in people at risk for developing Alzheimer's Disease and its related dementias (AD/ADRD), which are associated with high brain β-amyloid (Aβ) and hyperphosphorylated tau (tau-P) protein levels. Supraphysiologic-dose AAS induces androgen abnormalities and excess oxidative stress, which have been linked to increased and decreased expression or activity of proteins that synthesize and eliminate, respectively, Aβ and tau-P. Aβ and tau-P accumulation may begin soon after initiating supraphysiologic-dose AAS use, which typically occurs in the early 20s, and their accumulation may be accelerated by other psychoactive substance use, which is common among non-medical AAS users. Accordingly, the widespread use of supraphysiologic-dose AAS may increase the numbers of people who develop dementia. Early diagnosis and correction of sex-steroid level abnormalities and excess oxidative stress could attenuate risk for developing AD/ADRD in supraphysiologic-dose AAS users, in people with other substance use disorders, and in people with low sex-steroid levels or excess oxidative stress associated with aging.

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“…Cytosolic enzymes such as xanthine oxidase (XO) during the catalytic oxidation of hypoxanthine to xanthine and Prostaglandin H Synthase (PHS) from arachidonic acid to prostaglandin generate ROS [ 24 ]. In addition, environmental pollutants; ionizing radiation (UV-rays, X-rays, γ-rays, and infrared or electromagnetic waves); smoking; long-term chemical exposure like pesticides, insecticides, or industrial solvents; heavy or transition metals (Cu, Fe, Mn, As, Cd, Pb, and Hg); diet; and physical exercise contribute to the production of ROS/RNS [ 26 , 27 , 28 , 29 , 30 , 31 , 32 , 33 , 34 , 35 , 36 , 37 , 38 , 39 ].…”

Section: Introductionmentioning

confidence: 99%

Antioxidant Therapy in Oxidative Stress-Induced Neurodegenerative Diseases: Role of Nanoparticle-Based Drug Delivery Systems in Clinical Translation

et al. 2022

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Free radicals are formed as a part of normal metabolic activities but are neutralized by the endogenous antioxidants present in cells/tissue, thus maintaining the redox balance. This redox balance is disrupted in certain neuropathophysiological conditions, causing oxidative stress, which is implicated in several progressive neurodegenerative diseases. Following neuronal injury, secondary injury progression is also caused by excessive production of free radicals. Highly reactive free radicals, mainly the reactive oxygen species (ROS) and reactive nitrogen species (RNS), damage the cell membrane, proteins, and DNA, which triggers a self-propagating inflammatory cascade of degenerative events. Dysfunctional mitochondria under oxidative stress conditions are considered a key mediator in progressive neurodegeneration. Exogenous delivery of antioxidants holds promise to alleviate oxidative stress to regain the redox balance. In this regard, natural and synthetic antioxidants have been evaluated. Despite promising results in preclinical studies, clinical translation of antioxidants as a therapy to treat neurodegenerative diseases remains elusive. The issues could be their low bioavailability, instability, limited transport to the target tissue, and/or poor antioxidant capacity, requiring repeated and high dosing, which cannot be administered to humans because of dose-limiting toxicity. Our laboratory is investigating nanoparticle-mediated delivery of antioxidant enzymes to address some of the above issues. Apart from being endogenous, the main advantage of antioxidant enzymes is their catalytic mechanism of action; hence, they are significantly more effective at lower doses in detoxifying the deleterious effects of free radicals than nonenzymatic antioxidants. This review provides a comprehensive analysis of the potential of antioxidant therapy, challenges in their clinical translation, and the role nanoparticles/drug delivery systems could play in addressing these challenges.

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Nicotine and cigarette smoke modulate Nrf2-BDNF-dopaminergic signal and neurobehavioral disorders in adult rat cerebral cortex^#

Cited by 16 publications

References 76 publications

Cognition, serum BDNF levels, and BDNF Val66Met polymorphism in type 2 diabetes patients and healthy controls

Cognition, serum BDNF levels, and BDNF Val66Met polymorphism in type 2 diabetes patients and healthy controls

Supraphysiologic-dose anabolic–androgenic steroid use: A risk factor for dementia?

Antioxidant Therapy in Oxidative Stress-Induced Neurodegenerative Diseases: Role of Nanoparticle-Based Drug Delivery Systems in Clinical Translation

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Nicotine and cigarette smoke modulate Nrf2-BDNF-dopaminergic signal and neurobehavioral disorders in adult rat cerebral cortex#

Cited by 16 publications

References 76 publications

Cognition, serum BDNF levels, and BDNF Val66Met polymorphism in type 2 diabetes patients and healthy controls

Cognition, serum BDNF levels, and BDNF Val66Met polymorphism in type 2 diabetes patients and healthy controls

Supraphysiologic-dose anabolic–androgenic steroid use: A risk factor for dementia?

Antioxidant Therapy in Oxidative Stress-Induced Neurodegenerative Diseases: Role of Nanoparticle-Based Drug Delivery Systems in Clinical Translation

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Nicotine and cigarette smoke modulate Nrf2-BDNF-dopaminergic signal and neurobehavioral disorders in adult rat cerebral cortex^#