Nicotine promotes survival of cells expressing amyloid precursor protein and presenilin: Implication for Alzheimer's disease

Brown, Diane R.; Ramlochansingh, Carlana; Manaye, Kebreten F.; Tizabi, Yousef

doi:10.1016/j.neulet.2012.12.046

Cited by 11 publications

(4 citation statements)

References 33 publications

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“…Because AD is characterized by a deficit of cholinergic function, several cholinergic drugs have been tested including nicotine. Nicotine improved cognitive processes such as attention in rodents (Decker et al, 1992 ) and may be neuroprotective against Aβ toxicity (Brown et al, 2013 ). The activation of the α7 nicotinic acetylcholine receptor/phosphatidylinositol 3-kinase (α7nAChR/PI3K) signaling pathway and a cross talk with the Wnt signaling pathway seems to mediate nicotine's positive effects on memory impairment in TgAPPswe/PS1dE9 mice (Inestrosa et al, 2013 ).…”

Section: Discussionmentioning

confidence: 99%

Cotinine halts the advance of Alzheimer's disease-like pathology and associated depressive-like behavior in Tg6799 mice

Patel

Grizzell

Holmes

et al. 2014

Front. Aging Neurosci.

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Alzheimer's disease (AD) is associated with cognitive and non-cognitive symptoms for which there are currently no effective therapies. We have previously reported that cotinine, a natural product obtained from tobacco leaves, prevented memory loss and diminished amyloid-β (Aβ) plaque pathology in transgenic 6799 mice (Tg6799 mice) when treated prior to the development of the pathology. We have also shown that cotinine reduces depressive-like behavior in normal and chronically stressed C57BL/6 mice. Here, we extend our previous studies by investigating the effects of cotinine on the progression of AD-like pathology, depressive-like behavior, and the mechanisms underlying its beneficial effects in Tg6799 mice when left untreated until after a more advanced stage of the disease's development. The results show that vehicle-treated Tg6799 mice displayed an accentuated loss of working memory and an abundant Aβ plaque pathology that were accompanied by higher levels of depressive-like behavior as compared to control littermates. By contrast, prolonged daily cotinine treatment to Tg6799 mice, withheld until after a mid-level progression of AD-like pathology, reduced Aβ levels/plaques and depressive-like behavior. Moreover, this treatment paradigm dramatically improved working memory as compared to control littermates. The beneficial effects of cotinine were accompanied by an increase in the expression of the active form of protein kinase B and the postsynaptic density protein 95 in the hippocampi and frontal cortices of Tg6799 mice. This suggests that cotinine halts the progression of AD-like pathology while reducing depressive-like behavior by stimulating signaling pathways supporting synaptic plasticity in Tg6799 mice. The potential use of cotinine to treat cognitive and non-cognitive symptoms of AD is discussed.

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Section: Discussionmentioning

confidence: 99%

Cotinine halts the advance of Alzheimer's disease-like pathology and associated depressive-like behavior in Tg6799 mice

Patel

Grizzell

Holmes

et al. 2014

Front. Aging Neurosci.

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“…In vivo also, nicotine induces a change in the volume of astrocytes in the prefrontal cortex, CA1 of the hippocampus, and the substantia nigra. These and other findings indicate potential use of nicotine in neurodegenerative diseases including AD [10,64,65]. However, mode of nicotine administration appears to be an important factor in its therapeutic application.…”

Section: Ach-achrs: Astrocytesmentioning

confidence: 80%

Central Nicotinic and Muscarinic Receptors in Health and Disease

Tizabi¹,

Getachew²,

Tsytsarev³

et al. 2023

Acetylcholine - Recent Advances and New Perspectives

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Without acetylcholine (ACh) no skeletal muscle contraction, no preganglionic sympathetic or parasympathetic activity can be obtained. This can result in dysregulation of cardiac, respiratory, gastrointestinal, and renal functions as well as disruption of fluid secretion from various glands such as tears, saliva, digestive juices, sweat, and milk. Importantly, ACh deficiency in the brain can have severe cognitive consequences. The action of ACh is mediated by two distinct classes of receptors, namely the muscarinic (mAChRs), which are G-protein coupled (metabotropic) receptors and nicotinic receptors (nAChRs), which are ligand-gated ion channels (ionotropic receptors). The focus of this chapter is on interaction of these two distinct receptor classes and its implication in health and disease. Thus, following a brief description of ACh actions and its central circuitry, an update on mAChRs and nAChRs and how their interaction may impact neuropsychiatric/neurodegenerative diseases will be provided. Moreover, potential novel therapeutic intervention based on these interactions, particularly in relationship to Alzheimer’s and Parkinson’s diseases will be touched upon.

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“…Immature neurons derived from ongoing neurogenesis within the DG contain α7 nAChRs and receive direct cholinergic innervation that is critical for integration of these adult-born neurons into the DG network [ 67 ]. Nicotine has demonstrated neuroprotective abilities upon binding nAChRs on numerous cells throughout the brain, acting therapeutically by inducing defense mechanisms against pathology causing Alzheimer’s disease (AD) [ 70 , 71 ], Parkinson’s disease (PD) [ 20 , 72 , 73 , 74 , 75 , 76 ] and other neuroinflammatory conditions. Nicotine’s actions on hippocampal α7 nAChRs has been shown to prevent synaptic impairment induced by Aß oligomers through activation of phosphatidylinositol-3-kinase (PI3K) signaling pathways [ 77 ] ( Table 3 ).…”

Section: Nicotine Attenuates Aß-induced Neurotoxicity In Nscsmentioning

confidence: 99%

Systematic Review of Nicotine Exposure’s Effects on Neural Stem and Progenitor Cells

Brooks

Henderson

2021

Brain Sciences

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While various modalities of chronic nicotine use have been associated with numerous negative consequences to human health, one possible benefit of nicotine exposure has been uncovered. The discovery of an inverse correlation between smoking and Parkinson’s disease, and later Alzheimer’s disease as well, motivated investigation of nicotine as a neuroprotective agent. Some studies have demonstrated that nicotine elicits improvements in cognitive function. The hippocampus, along with the subventricular zone (SVZ), is a distinct brain region that allow for ongoing postnatal neurogenesis throughout adulthood and plays a major role in certain cognitive behaviors like learning and memory. Therefore, one hypothesis underlying nicotine-induced neuroprotection is possible effects on neural stem cells and neural precursor cells. On the other hand, nicotine withdrawal frequently leads to cognitive impairments, particularly in hippocampal-dependent behaviors, possibly suggesting an impairment of hippocampal neurogenesis with nicotine exposure. This review discusses the current body of evidence on nicotine’s effects on neural stem cells and neural progenitors. Changes in neural stem cell proliferation, survival, intracellular dynamics, and differentiation following acute and chronic nicotine exposure are examined.

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Nicotine promotes survival of cells expressing amyloid precursor protein and presenilin: Implication for Alzheimer's disease

Cited by 11 publications

References 33 publications

Cotinine halts the advance of Alzheimer's disease-like pathology and associated depressive-like behavior in Tg6799 mice

Cotinine halts the advance of Alzheimer's disease-like pathology and associated depressive-like behavior in Tg6799 mice

Central Nicotinic and Muscarinic Receptors in Health and Disease

Systematic Review of Nicotine Exposure’s Effects on Neural Stem and Progenitor Cells

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