Nicotine reduces Aβ in the brain and cerebral vessels of APPsw mice

Hellström‐Lindahl, Ewa; Court, Jennifer A.; Keverne, Jessica; Svedberg, Marie; Lee, Mandy; Marutle, Amelia; Thomas, Alan; Perry, Elaine K.; Bednar, I.; Nordberg, Agneta

doi:10.1111/j.0953-816x.2004.03377.x

Cited by 110 publications

(18 citation statements)

References 52 publications

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“…( 4B ) [20]. The increased basal protein levels of BDNF in area CA1 of Aβ-infused rats is in agreement with an earlier report that shows an increase in the protein levels of BDNF in the forebrain in APPsw mice [90]. …”

Section: Chronic Stress Accentuates Altered Levels Of Signaling Molecsupporting

confidence: 88%

“…Furthermore, as chronic nicotine treatment is known to upregulate BDNF protein level and mRNA expression in area CA1 [9, 90], it is not surprising that BDNF protein levels are significantly increased in nicotine, nicotine/Aβ, and nicotine/stress/Aβ rats, compared to control rats Fig. ( 4B ).…”

Section: Chronic Stress Accentuates Altered Levels Of Signaling Molecmentioning

confidence: 99%

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Chronic Stress and Alzheimers Disease-Like Pathogenesis in a Rat Model: Prevention by Nicotine

Alkadhi¹

2011

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Environmental factors including chronic stress may play a critical role in the manifestation of Alzheimer’s disease (AD).This review summarizes our studies of the aggravation of the impaired cognitive ability and its cellular and molecular correlates by chronic psychosocial stress and prevention by nicotine in an Aβ rat model of AD. We utilized three approaches: learning and memory tests in the radial arm water maze, electrophysiological recordings of the cellular correlates of memory, long-term potentiation (LTP) and long-term depression (LTD), in anesthetized rats, and immunoblot analysis of synaptic plasticity- and cognition-related signaling molecules. The Aβ rat model, representing the sporadic form of established AD, was induced by continuous i.c.v. infusion of a pathogenic dose of Aβ peptides via a 14- day osmotic pump. In this AD model, chronic stress intensified cognitive deficits, accentuated the disruption of signaling molecules levels and produced greater depression of LTP than what was seen with Aβ infusion alone. Chronic treatment with nicotine was highly efficient in preventing the effects of Aβ infusion and the exacerbating impact of chronic stress. Possible mechanisms for the effect of chronic stress are discussed.

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Section: Chronic Stress Accentuates Altered Levels Of Signaling Molecsupporting

confidence: 88%

Section: Chronic Stress Accentuates Altered Levels Of Signaling Molecmentioning

confidence: 99%

Chronic Stress and Alzheimers Disease-Like Pathogenesis in a Rat Model: Prevention by Nicotine

Alkadhi¹

2011

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“…Attenuation of elevated [ 125 ]-abungarotoxin binding (a7) in APPsw mice was observed after 5.5 months nicotine treatment. Both these observations suggest that the reduction in insoluble Ab by nicotine might be in part mediated via the a7 nicotine receptor [66].…”

Section: Nicotinementioning

confidence: 88%

Natural Antioxidants Protect Neurons in Alzheimer’s Disease and Parkinson’s Disease

Zhao

2009

Neurochem Res

166

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"Modern" medicine and pharmacology require an effective medical drug with a single compound for a specific disease. This seams very scientific but usually has unavoidable side effects. For example, the chemical therapy to cancer can totally damage the immunological ability of the patient leading to death early than non-treatment. On the other hand, natural antioxidant drugs not only can cure the disease but also can enhance the immunological ability of the patient leading to healthier though they usually have several compounds or a mixture. For the degenerative disease such as Alzheimer's disease (AD) and Parkinson's disease (PD), natural antioxidant drugs are suitable drugs, because the pathogenesis of these diseases is complex with many targets and pathways. These effects are more evidence when the clinic trial is for long term treatment. The author reviews the studies on the protecting effects of natural antioxidants on neurons in neurodegenerative diseases, especially summarized the results about protective effect of green tea polyphenols on neurons against apoptosis of cellular and animal PD models, and of genestine and nicotine on neurons against A beta-induced apoptosis of hippocampal neuronal and transgenic mouse AD models.

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“…Furthermore, pharmacological modulation of α7 nAChR also has some potential promise as a neuroprotective strategy (Kihara et al, 2001; Hellstrom-Lindahl et al, 2004; Hu et al, 2007; Roncarati et al, 2009). The current over-arching view is that increasing activity of α7 nAChRs is the required route to improved cognitive function, a supposition that is supported by behavioral data using agonists, and to a lesser extent PAMs.…”

Section: Discussionmentioning

confidence: 99%

Voltage- and Temperature-Dependent Allosteric Modulation of α7 Nicotinic Receptors by PNU120596

Sitzia¹,

Brown²,

Randall³

et al. 2011

Front. Pharmacol.

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Alpha7 nicotinic acetylcholine receptors (α7 nAChR) are widely distributed throughout the central nervous system and are found at particularly high levels in the hippocampus and cortex. Several lines of evidence indicate that pharmacological enhancement of α7 nAChRs function could be a potential therapeutic route to alleviate disease-related cognitive deficits. A recent pharmacological approach adopted to increase α7 nAChR activity has been to identify selective positive allosteric modulators (PAMs). α7 nAChR PAMs have been divided into two classes: type I PAMs increase agonist potency with only subtle effects on kinetics, whereas type II agents produce additional dramatic effects on desensitization and deactivation kinetics. Here we report novel observations concerning the pharmacology of the canonical type II PAM, PNU120596. Using patch clamp analysis of acetylcholine (ACh)-mediated currents through recombinant rat α7 nAChR we show that positive allosteric modulation measured in two different ways is greatly attenuated when the temperature is raised to near physiological levels. Furthermore, PNU120596 largely removes the strong inward rectification usually exhibited by α7 nAChR-mediated responses.

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Nicotine reduces Aβ in the brain and cerebral vessels of APPsw mice

Cited by 110 publications

References 52 publications

Chronic Stress and Alzheimers Disease-Like Pathogenesis in a Rat Model: Prevention by Nicotine

Chronic Stress and Alzheimers Disease-Like Pathogenesis in a Rat Model: Prevention by Nicotine

Natural Antioxidants Protect Neurons in Alzheimer’s Disease and Parkinson’s Disease

Voltage- and Temperature-Dependent Allosteric Modulation of α7 Nicotinic Receptors by PNU120596

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