path(MESH:Anxiety)
In particular, repeated self-administration produces the upregulation of high-affinity (alpha4beta2) nAChR expression, reduces receptor function due to desensitization and, in most cases, imparts developmental tolerance. Additional changes imposed by nicotine abuse range from reinforcement to physical discomfort associated with withdrawal including craving, anxiety, and a multitude of other less than desirable sensations of autonomic dysfunction when use is stopped. PubMed:19126755
Genetic evidence has linked nicotinic receptors to epilepsy and schizophrenia, and studies with mutant mice have implicated nAChRs in pain mechanisms, anxiety, and depression. PubMed:17009926
AD is the most commonly diagnosed form of dementia and currently affects approximately 35 million individuals worldwide.7 AD is a progressive neurodegenerative disease that is characterized by a host of cognitive deficits, including impairments in learning and memory. In addition to the well-documented cognitive impairments, AD patients also display behavioral disturbances, including anxiety, depression, and psychosis PubMed:24511233
We finally measured anxiety levels using the LDB paradigm. No differences were observed between both groups for the index of time spent in the lit compartment (p = 0.7) as well as for the number of transitions (p = 0.2; Fig. 2GeH) PubMed:27522251
In 2011, we know that cholinergic actions in the brain govern various processes: cognition (attention and executive function) (Couey et al., 2007; Levin and Rezvani, 2007; Heath and Picciotto, 2009; Howe et al., 2010), learning and memory (Gould, 2006; Couey et al., 2007; Levin and Rezvani, 2007), mood (anxiety, depression) (Picciotto et al., 2008), reward (addiction, craving) (Tang and Dani, 2009), and sensory processing (Heath and Picciotto, 2009) PubMed:21482353
The nAChRs are found to be involved in a complex range of central nervous system disorders including Alzheimer’s disease (AD), Parkinson’s disease, schizophrenia, Tourette’s syndrome, anxiety, depression, and epilepsy (Newhouse and Kelton 2000; Newhouse et al 1997; Paterson and Nordberg 2000) PubMed:11230871
nAChRs contribute to cognitive function, and changes in their number and/or func- tion are associated with various pathological conditions such as cognitive disorders, anxiety, depression, Alzheimer’s and Parkinson’s disease, pain and epilepsy PubMed:28901280
Once in the bloodstream, nicotine, rapidly crosses the blood/brain barrier, and accumulates and exerts its pharmacological effects [9, 58] (including psy- chostimulation, reward and the reduction of stress and anxi- ety) in the brain by binding to nAChRs. PubMed:28901280
Treatment with Dyrk1A inhibitor, green tea flavonol epigallocatechin-gallate (EGCG), from gestation to adulthood suppressed 3R-tau expression and rescued anxiety and memory deficits in Ts65Dn mouse brains. PubMed:28775333
Treatment with Dyrk1A inhibitor, green tea flavonol epigallocatechin-gallate (EGCG), from gestation to adulthood suppressed 3R-tau expression and rescued anxiety and memory deficits in Ts65Dn mouse brains. PubMed:28775333
Tg Tau P301S mice treated with anatabine spent significantly more time (T-test, P<0.05) in the open arms of the elevated plus maze than placebo Tg Tau P301S mice (Figure 3). DOI:10.4172/2168-975X.1000126
(-)-Nicotine withdrawal symptoms might begin within a few hours after the last nicotine product, and include irritability/anger/stress/anxiety, sleep disturbances, depressed mood, craving, cognitive and attention deficits, and increased appetite. PubMed:28391535
Transgenic mouse models of AD overexpressing Aβ peptides generally show greater locomotor activity and disinhibition in the elevated plus maze compared to non-transgenic mice, suggest- ing hyperactivity and a lower level of anxiety [28–30]. PubMed:26010758
The disinhibition affecting Tg PS1/APPswe mice was suppressed following treatment with anatabine at a dosage of either 10 or 20 mg/Kg/Day at both the time points (Figs 2D and 3D). PubMed:26010758
p50 knock-out mice exhibit severe deficits in learning as assessed by an active avoidance assay [93] in addition to displaying lack of anxiety-like behavior in well-established tests and paradigms that assess exploratory drive as a measure of anxiety PubMed:28745240
Several present with obsessive compulsive behavior, mood disorder, a high anxiety level, temper tantrums, self-injurious and (verbally) aggressive behavior. PubMed:29724491
Genetic evidence has linked nicotinic receptors to epilepsy and schizophrenia, and studies with mutant mice have implicated nAChRs in pain mechanisms, anxiety, and depression. PubMed:17009926
In 2011, we know that cholinergic actions in the brain govern various processes: cognition (attention and executive function) (Couey et al., 2007; Levin and Rezvani, 2007; Heath and Picciotto, 2009; Howe et al., 2010), learning and memory (Gould, 2006; Couey et al., 2007; Levin and Rezvani, 2007), mood (anxiety, depression) (Picciotto et al., 2008), reward (addiction, craving) (Tang and Dani, 2009), and sensory processing (Heath and Picciotto, 2009) PubMed:21482353
The nAChRs are found to be involved in a complex range of central nervous system disorders including Alzheimer’s disease (AD), Parkinson’s disease, schizophrenia, Tourette’s syndrome, anxiety, depression, and epilepsy (Newhouse and Kelton 2000; Newhouse et al 1997; Paterson and Nordberg 2000) PubMed:11230871
nAChRs contribute to cognitive function, and changes in their number and/or func- tion are associated with various pathological conditions such as cognitive disorders, anxiety, depression, Alzheimer’s and Parkinson’s disease, pain and epilepsy PubMed:28901280
Treatment with Dyrk1A inhibitor, green tea flavonol epigallocatechin-gallate (EGCG), from gestation to adulthood suppressed 3R-tau expression and rescued anxiety and memory deficits in Ts65Dn mouse brains. PubMed:28775333
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