Genetic deletion of TRPA1 receptor attenuates amyloid beta- 1-42 (Aβ1-42)-induced neurotoxicity in the mouse basal forebrain in vivo
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چکیده
منابع مشابه
Treatment of beta amyloid 1–42 (Aβ1–42)-induced basal forebrain cholinergic damage by a non-classical estrogen signaling activator in vivo
In Alzheimer's disease (AD), there is a loss in cholinergic innervation targets of basal forebrain which has been implicated in substantial cognitive decline. Amyloid beta peptide (Aβ(1-42)) accumulates in AD that is highly toxic for basal forebrain cholinergic (BFC) neurons. Although the gonadal steroid estradiol is neuroprotective, the administration is associated with risk of off-target effe...
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Senile plaques are a hallmark of Alzheimer's disease (AD), a neurodegenerative disease associated with cognitive decline and aging. Abeta(1-42) is the primary component of the senile plaque in AD brain and has been shown to induce protein oxidation in vitro and in vivo. Oxidative stress is extensive in AD brain. As a result, Abeta(1-42) has been proposed to play a central role in the pathogenes...
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Amyloid β-peptide (Aβ) is thought by many researchers to be central to the pathogenesis of Alzheimer’s disease (AD) (reviewed in Ref. 1). In addition, oxidative stress, manifested by protein oxidation and lipid peroxidation, is apparent in AD brain.2,3 Our laboratory developed a comprehensive hypothesis for neurotoxicity in AD brain that unites these two observations and provides a testable fra...
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Amyloid beta-peptide (1-42) [Abeta(1-42)] has been proposed to play a central role in the pathogenesis of Alzheimer's disease, a neurodegenerative disorder associated with cognitive decline and aging. AD brain is under extensive oxidative stress, and Abeta(1-42) has been shown to induce protein oxidation, lipid peroxidation, and reactive oxygen species formation in neurons and synaptosomes, all...
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ژورنال
عنوان ژورنال: Mechanisms of Ageing and Development
سال: 2020
ISSN: 0047-6374
DOI: 10.1016/j.mad.2020.111268