Beta-amyloid exhibits antagonistic effects on alpha 7 nicotinic acetylcholine receptors in orchestrated manner

Sadigh-Eteghad, Saeed; Talebi, Mahnaz; Farhoudi, Mehdi; Golzari, Samad Ej; Sabermarouf, Babak; Mahmoudi, Javad

doi:10.1016/j.jmhi.2014.01.001

Cited by 34 publications

(29 citation statements)

References 36 publications

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“…Ab either activates or inhibits a 7 nAChRs in a dosedependent manner (Oz et al 2013;Sadigh-Eteghad et al 2014). Picomolar Ab doses which exist in vivo in the healthy brain enhance spontaneous astrocyte calcium transients.…”

Section: Ad and Astrocytic Nachrsmentioning

confidence: 99%

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Astrocytic and microglial nicotinic acetylcholine receptors: an overlooked issue in Alzheimer’s disease

et al. 2016

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It is increasingly recognized that astrocytes and microglia-associated dysfunction contribute to AD pathology. In addition, glial nicotinic acetylcholine receptors (nAChRs) play a role in AD-related phenomena, such as neuron survival, synaptic plasticity, and memory. From mechanistic point of view, the glial regulation of pro-inflammatory cytokines, as common contributors in AD, is modulated by nAChRs. Astrocytic and microglial nAChRs contribute to Aβ metabolism, including Aβ phagocytosis and degradation as well as Aβ-related oxidative stress and neurotoxicity. These receptors are also involved in neurotransmission and gliotransmission through indirect interaction with N-Methyl-D-aspartate (NMDA) and a-amino-3-hydroxy-5-methyl-4 isoxazolepropionic acid (AMPA) receptors as well as gamma-aminobutyric acid (GABA) and intracellular calcium regulation. In addition, glial nAChRs participate in trophic factors-induced neuroprotection. This review gathers the most recent advances along with the previous data on astrocytic and microglial nAChRs role in AD pathogenesis.

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Section: Ad and Astrocytic Nachrsmentioning

confidence: 99%

“…Receptors residing on glial cells have some physiological role in glial function (Sharma and Vijayaraghavan 2001;Shytle et al 2006;Volterra and Meldolesi 2005). In addition, these receptors are important in AD pathogenesis and treatment (Sadigh-Eteghad et al 2014, 2015a specially those which reside on glial cells (Tuppo and Arias 2005).…”

Section: Introductionmentioning

confidence: 99%

Astrocytic and microglial nicotinic acetylcholine receptors: an overlooked issue in Alzheimer’s disease

et al. 2016

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“…Memory and cognitive impairment due to the progressive loss of neurons is considered the hallmark of AD-type dementia [1-4]. From the histopathological point of view, AD progression is mostly associated with the extracellular deposition of beta amyloid (Aβ) peptides [5]. Evidence supports that Aβ plays the main role in the cholinergic dysfunction during AD [6].…”

Section: Introductionmentioning

confidence: 99%

Exercise Improves Recognition Memory and Acetylcholinesterase Activity in the Beta Amyloid-Induced Rat Model of Alzheimer’s Disease

et al. 2018

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Objective: A correlation between physical exercise and cognitive improvement has been found in Alzheimer’s disease (AD). This study aimed to investigate the effects of aerobic and resistance exercise on the recognition memory and acetylcholinesterase (AChE) activity in beta amyloid (Aβ) model of AD in rat. Materials and Methods: Fifty male 8-week-old Wistar rats (250–280 g) were divided into 5 groups (n = 10 each) of control, sham surgery, Aβ-received sedentary, Aβ-received with aerobic exercise and Aβ-received with resistance exercise. AD was induced by intracerebroventricular injection of Aβ_25–35 peptide. The sham surgery group received normal saline using the same route and condition. Two groups of Aβ-received animals were trained by treadmill for aerobic exercise and by ladder for strength exercise for 8 weeks (4 days/week). Novel object recognition (NOR) task was used to assess recognitional memory in groups. AChE activity in the brain tissue was assessed using the Spectrophotometry method. Results: There was no significant difference in memory index and AChE activity between the sham surgery and control groups (p > 0.05). Also, impairment of NOR indices was seen in the Aβ-injected sedentary rats (p < 0.05). However, both aerobic and strength training improved the exploration index in this test (p < 0.05). Further, AChE activity increased in the Aβ-injected sedentary group but declined in the aerobic and resistance exercise groups (p < 0.01). Conclusion: Aerobic and resistance exercise could improve recognition memory and decrease AChE activity in Aβ-induced AD in rats. The decrease in AChE activity may be one of the mechanisms by which exercise improves cognition and memory in AD.

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“…According to the 2010 World Alzheimer's Report, more than 36 million people are living with dementia, and it is expected that this number will be tripled by 2050 (40,48). Cognitive decline, a major symptom exhibited by patients with AD, is associated with amyloid-beta (Aβ) deposition in the brain tissue (42,43).…”

Section: Introductionmentioning

confidence: 99%

Intranasal insulin treatment improves memory and learning in a rat amyloid-beta model of Alzheimer’s disease

Farzampour¹,

Majdi²,

Sadigh-Eteghad³

2016

Physiology International

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Recently, insulin has been used as a pro-cognitive agent for the potential treatment of Alzheimer's disease (AD), because of its ability to cross the brain-blood barrier (BBB) by a saturable transport system. This study has been designed to evaluate the effects of intranasal insulin regimen, as a bypass system of BBB, on spatial memory in amyloid-beta (Aβ) model of AD in rat. Unilateral infusion of Aβ 25-35 (10 nmol/2 μl/rat) into the lateral ventricular region of brain was used to produce a rat model of AD. After a 24-h recovery period, rats received insulin or vehicle via intraperitoneal or intranasal route (0.1, 0.2, and 0.3 IU) for 14 days. Memory function in rats was assessed by Morris water maze test, with 5 days of training and consequent probe test protocol. Different doses of intraperitoneal insulin did not have a significant effect on learning and memory in AD rats. However, intranasal insulin at doses of 0.2 and 0.3 IU improved the learning and memory in Aβ-received rats.In conclusion, intranasal insulin as a non-invasive strategy improves spatial learning and memory in AD model.

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Beta-amyloid exhibits antagonistic effects on alpha 7 nicotinic acetylcholine receptors in orchestrated manner

Cited by 34 publications

References 36 publications

Astrocytic and microglial nicotinic acetylcholine receptors: an overlooked issue in Alzheimer’s disease

Astrocytic and microglial nicotinic acetylcholine receptors: an overlooked issue in Alzheimer’s disease

Exercise Improves Recognition Memory and Acetylcholinesterase Activity in the Beta Amyloid-Induced Rat Model of Alzheimer’s Disease

Intranasal insulin treatment improves memory and learning in a rat amyloid-beta model of Alzheimer’s disease

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