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amyotrophic lateral sclerosis/nicotina
L'enllaç es desa al porta-retalls
Pàgina 1 des de 16 resultats
Trafficking of alpha4* nicotinic receptors revealed by superecliptic phluorin: effects of a beta4 amyotrophic lateral sclerosis-associated mutation and chronic exposure to nicotine.
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We employed a pH-sensitive GFP analog, superecliptic phluorin, to observe aspects of nicotinic acetylcholine receptor (nAChR) trafficking to the plasma membrane (PM) in cultured mouse cortical neurons. The experiments exploit differences in the pH among endoplasmic reticulum (ER), trafficking
Habenular expression of rare missense variants of the β4 nicotinic receptor subunit alters nicotine consumption.
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The CHRNA5-CHRNA3-CHRNB4 gene cluster, encoding the α5, α3, and β4 nicotinic acetylcholine receptor (nAChR) subunits, has been linked to nicotine dependence. The habenulo-interpeduncular (Hb-IPN) tract is particularly enriched in α3β4 nAChRs. We recently showed that modulation of these receptors in
Rare missense variants of neuronal nicotinic acetylcholine receptor altering receptor function are associated with sporadic amyotrophic lateral sclerosis.
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Sporadic amyotrophic lateral sclerosis (SALS) is a motor neuron degenerative disease of unknown etiology. Current thinking on SALS is that multiple genetic and environmental factors contribute to disease liability. Since neuronal acetylcholine receptors (nAChRs) are part of the glutamatergic
Mutant human β4 subunit identified in amyotrophic lateral sclerosis patients impairs nicotinic receptor function.
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Recently identified mutations in the genes encoding the neuronal nicotinic ACh receptor (nAChR) subunits in patients affected by sporadic amyotrophic lateral sclerosis (sALS) may represent a factor which enhances disease susceptibility, in particular in association with ambient causes such as
Smoking, snuff dipping and the risk of amyotrophic lateral sclerosis--a prospective cohort study.
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BACKGROUND
Little is known about the etiology of amyotrophic lateral sclerosis (ALS). The association between cigarette smoking, but not other types of smoking and snuff dipping, and the risk of ALS has been evaluated in several epidemiologic studies. The findings were inconclusive.
METHODS
We
Amyotrophic Lateral Sclerosis: An update for 2013 Clinical Features, Pathophysiology, Management and Therapeutic Trials.
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Amyotrophic lateral sclerosis (ALS), first described by Jean-Martin Charcot in the 1870s, is an age-related disorder that leads to degeneration of motor neurons. The disease begins focally in the central nervous system and then spreads relentlessly. The clinical diagnosis, defined by progressive
Nicotine protects rat hypoglossal motoneurons from excitotoxic death via downregulation of connexin 36.
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Motoneuron disease including amyotrophic lateral sclerosis may be due, at an early stage, to deficit in the extracellular clearance of the excitatory transmitter glutamate. A model of glutamate-mediated excitotoxic cell death based on pharmacological inhibition of its uptake was used to investigate
Factors correlated with hypermetabolism in patients with amyotrophic lateral sclerosis.
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BACKGROUND
Amyotrophic lateral sclerosis (ALS) is a severe disease characterized by neurogenic amyotrophy and degeneration of upper and lower motor neurons. Although ALS patients usually experience reductions in fat-free mass (FFM), hypermetabolism via an undetermined source has also been
The cholinergic anti-inflammatory system limits T cell infiltration into the neurodegenerative CNS, but cannot counteract complex CNS inflammation.
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Stimulation of the nicotinic alpha7 acetylcholine receptor (nAChRalpha7) by nicotine or acetylcholine initiates the cholinergic anti-inflammatory pathway, a mechanism for neural inhibition of inflammation. The action of this pathway was initially discovered in animal models of endotoxemia and septic
Nicotinic receptor activation contrasts pathophysiological bursting and neurodegeneration evoked by glutamate uptake block on rat hypoglossal motoneurons.
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Impaired uptake of glutamate builds up the extracellular level of this excitatory transmitter to trigger rhythmic neuronal bursting and delayed cell death in the brainstem motor nucleus hypoglossus. This process is the expression of the excitotoxicity that underlies motoneuron degeneration in
A "two-hit" hypothesis for inclusion formation by carboxyl-terminal fragments of TDP-43 protein linked to RNA depletion and impaired microtubule-dependent transport.
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Carboxyl-terminal fragments (CTFs) of TDP-43 aggregate to form the diagnostic signature inclusions of frontotemporal lobar degeneration and amyotrophic lateral sclerosis, but the biological significance of these CTFs and how they are generated remain enigmatic. To address these issues, we engineered
[Chronic phosphoproteomic in temporal lobe epilepsy mouse models induced by kainic acid].
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METHODS
Kainic acid-induced temporal lobe epilepsy models were conducted, when reaching stage 4Conditions Associated with Essential Tremor in Veterans: A Potential Role for Chronic Stress.
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Increased depression, hearing loss, dementia, alcoholism, and mortality in essential tremor patients remain unexplained. We investigated whether conditions associated with tremor are linked to chronic stress.
The FY2013 Veterans Affairs database was queried for 38 selected dual diagnosis
Clinical trials of N-acetylcysteine in psychiatry and neurology: A systematic review.
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N-acetylcysteine (NAC) is recognized for its role in acetaminophen overdose and as a mucolytic. Over the past decade, there has been growing evidence for the use of NAC in treating psychiatric and neurological disorders, considering its role in attenuating pathophysiological processes associated
Physiological characterization of human muscle acetylcholine receptors from ALS patients.
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Amyotrophic lateral sclerosis (ALS) is characterized by progressive degeneration of motor neurons leading to muscle paralysis. Research in transgenic mice suggests that the muscle actively contributes to the disease onset, but such studies are difficult to pursue in humans and in vitro models would
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