Nicotine modulates the neurotoxic effect of β-amyloid protein(25–35) in hippocampal cultures

Zamani, Maryam; Allen, Y.S.; Gill, Owen; Gray, Jeffrey A.

doi:10.1097/00001756-199701200-00027

Cited by 87 publications

(47 citation statements)

References 13 publications

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“…35 Nicotinic receptor stimulation, especially α7nAChR activation by treatment with nicotine as an example, protects neuron against Aβ-induced cytotoxicity both in cortical and hippocampal neurons. 36,37 Furthermore, we here demonstrated described with some modifications. 14 Briefly, the brain tissues were cleaned free of meningeal tissue, minced and mechanically dissociated by passage through a flame-polished Pasteur pipette.…”

Section: Methodsmentioning

confidence: 91%

Autophagy protects neuron from Aβ-induced cytotoxicity

Hung

Huang²,

Liou³

et al. 2009

Autophagy

166

139

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Autophagy is a degradation pathway for the turnover of dysfunctional organelles or aggregated proteins in cells. Extracellular accumulation of β-amyloid peptide has been reported to be a major cause of Alzheimer disease (AD) and large numbers of autophagic vacuoles accumulate in the brain of AD patient. However, how autophagic process is involved in Aβ-induced neurotoxicity and how Aβ peptide is transported into the neuron and metabolized is still unknown. In order to study the role of autophagic process in Aβ-induced neurotoxicity, EGFP-LC3 was overexpressed in On the other hand, nicotine (nAChR agonist) enhanced the autophagic process and also inhibited cell death following Aβ application. In addition, nicotine but not α-BTX increased primary hippocampal neuronal survival following Aβ treatment. Furthermore, using Atg7 siRNA to inhibit autophagosome formation in an early step or α7nAChR siRNA to knock down α7nAChR significantly enhanced Aβ-induced neurotoxicity. Confocal double-staining imaging shows that nicotine treatment in the presence of Aβ enhanced the colocalization of α7nAChR with autophagosomes. These results suggest that α7nAChR may act as a carrier to bind with eAβ and internalize into cytoplasm and further inhibit Aβ-induced neurotoxicity via autophagic degradation pathway. Our results suggest that autophagy process plays a neuroprotective role against Aβ-induced neurotoxicity. Defect in autophagic regulation or Aβ-α7nAChR transport system may impair the clearance of Aβ and enhance neuronal death. SH-SY5Y cells (SH-SY5Y/pEGFP-LC3). It was found that treatment with

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Section: Methodsmentioning

confidence: 91%

Autophagy protects neuron from Aβ-induced cytotoxicity

Hung

Huang²,

Liou³

et al. 2009

Autophagy

166

139

View full text Add to dashboard Cite

show abstract

“…More recent studies have shown that nicotine can protect against toxicity induced by ␤-amyloid [A␤, the amyloidogenic fragment of the amyloid precursor protein, (APP)], the primary component of neuritic plaques found in the brains of patients with AD (Kihara et al, 1997(Kihara et al, , 1998Zamani et al, 1997) (Table 1). Interestingly, both ␣-bungarotoxin sensitive and insensitive nAChRs are effective in these in vitro models.…”

Section: Neuronal Nachrs and Neuroprotectionmentioning

confidence: 99%

“…However, in many cases, the neuroprotective effects of nicotine can be blocked by mecamylamine or dihydro-␤-erythroidine, antagonists relatively selective for the high-affinity subfamily (mainly ␣4/␤2 subunit-containing) of nAChRs (Kaneko et al, 1997;Zamani et al, 1997;Kihara et al, 1998;Ryan et al, 2001;Laudenbach et al, 2002). The relative contribution of different nAChR subtypes may vary with brain regions such that cortical and striatal neuroprotection by nicotine may be mediated more through ␣4/␤2-type nAChRs (Ryan et al, 2001;Laudenbach et al, 2002), whereas nicotine-induced neuroprotection in the hippocampus and spinal cord may be mediated more through ␣7-type nAChRs (Messi et al, 1997;Dajas-Bailador et al, 2000).…”

Section: And In Vivomentioning

confidence: 99%

Nicotinic receptors in aging and dementia

2002

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Activation of neuronal nicotinic acetylcholine receptors (nAChRs) has been shown to maintain cognitive function following aging or the development of dementia. Nicotine and nicotinic agonists have been shown to improve cognitive function in aged or impaired subjects. Smoking has also been shown in some epidemiological studies to be protective against the development of neurodegenerative diseases. This is supported by animal studies that have shown nicotine to be neuroprotective both in vivo and in vitro. Treatment with nicotinic agonists may therefore be useful in both slowing the progression of neurodegenerative illnesses, and improving function in patients with the disease. While increased nicotinic function has been shown to be beneficial, loss of cholinergic markers is often seen in patients with dementia, suggesting that decreased cholinergic function could contribute to both the cognitive deficits, and perhaps the neuronal degeneration, associated with dementia. In this article we will review the literature on each of these areas. We will also present hypotheses that might address the mechanisms underlying the ability of nAChR function to protect against neurodegeneration or improve cognition, two potentially distinct actions of nicotine.

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“…Just like a number of tetracyclic and carbazole-type compounds, benzofuran inhibits Aβ fibril formation, as a result of the inhibitory properties of these compounds (Howlett et al, 1999). Nicotine can prevent the conformational transition from α-helix to β-sheet (Salomon et al, 1996), and attenuate the neurotoxicity of Aβ through the nicotine receptor (Zamani et al, 1997). Nicotine also enhances the biosynthesis and secretion of transthyretin, which could bind to Aβ peptide to inhibit the formation of amyloid deposition (Tsuzuki et al, 2000).…”

Section: Preventing Aβ Aggregation Formationmentioning

confidence: 99%