Brain cholinesterases: II. The molecular and cellular basis of Alzheimer's disease

Shen, Zheng-Xuan

doi:10.1016/j.mehy.2004.02.031

Cited by 52 publications

(28 citation statements)

References 87 publications

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“…The cholinergic hypothesis proposed that AD is caused by cholinergic effects such as reduced synthesis of the neurotransmitter acetylcholine, or the initiation of large-scale aggregation of amyloid and neuroinflammation [238,239] . Most currently available drug therapies are based on this hypothesis [240] .…”

Section: Non-aβ Hypothesismentioning

confidence: 99%

Amyloid beta: structure, biology and structure-based therapeutic development

et al. 2017

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Amyloid beta peptide (Aβ) is produced through the proteolytic processing of a transmembrane protein, amyloid precursor protein (APP), by β-and γ-secretases. Aβ accumulation in the brain is proposed to be an early toxic event in the pathogenesis of Alzheimer's disease, which is the most common form of dementia associated with plaques and tangles in the brain. Currently, it is unclear what the physiological and pathological forms of Aβ are and by what mechanism Aβ causes dementia. Moreover, there are no efficient drugs to stop or reverse the progression of Alzheimer's disease. In this paper, we review the structures, biological functions, and neurotoxicity role of Aβ. We also discuss the potential receptors that interact with Aβ and mediate Aβ intake, clearance, and metabolism. Additionally, we summarize the therapeutic developments and recent advances of different strategies for treating Alzheimer's disease. Finally, we will report on the progress in searching for novel, potentially effective agents as well as selected promising strategies for the treatment of Alzheimer's disease. These prospects include agents acting on Aβ, its receptors and tau protein, such as small molecules, vaccines and antibodies against Aβ; inhibitors or modulators of β-and γ-secretase; Aβ-degrading proteases; tau protein inhibitors and vaccines; amyloid dyes and microRNAs.

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Section: Non-aβ Hypothesismentioning

confidence: 99%

Amyloid beta: structure, biology and structure-based therapeutic development

et al. 2017

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“…Acetylcholinesterase (AChE) inhibition has been thought to be quite important for the reduction of activity of the cholinergic neurons detected in the brains of AD patients (Schmitz et al, 2004). AChE inhibitors diminish the rate at which acetylcholine (ACh) is broken down and hence increase the concentration of ACh in the brain (Shen, 2004;Samanta et al, 2006). The commercially available AChE inhibitors such as tacrine, donepezil, rivastigmine, or galanthamine may help to prevent, for a limited time, some symptoms from becoming worse for some people in the early and middle stages of the disease (Luckmann, 2006;Haviv et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

In vitro Anticholinesterase Activity of Various Alkaloids

Orhan

Naz

Kartal

et al. 2007

Zeitschrift Für Naturforschung C

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In the current study, a number of alkaloids including retamine, cytisine, and sparteine (quinolizidine-type), yohimbine and vincamine (indole-type), scopolamine and atropine (tropane-type), colchicine (tropolone-type), allantoin (imidazolidine-type), trigonelline (pyridine-type) as well as octopamine, synephrine, and capsaicin (exocyclic amine-type) were tested in vitro for their inhibitory activity against acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) at 1 mg/ml concentration by the Ellman method using an ELISA microplate reader. Among the alkaloids tested, only capsaicin exerted a remarkable inhibitory effect towards both AChE and BChE [(62.7 ð 0.79)% and (75.3 ð 0.98)%, respectively]. While the rest of the alkaloids did not show any significant inhibition against AChE, three of the alkaloids, namely retamine, sparteine, and yohimbine, exerted a noteworthy anti-BChE effect as compared to galanthamine, the reference drug.

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“…First, the cholinergic hypothesis is one of the oldest and most useful hypothesis on which current drug therapies are based for the management of AD [30]. It links cholinergic effects to aggregation of amyloids and inflammation of the neurons [31][32][33][34]. Secondly, amyloid hyponthesis suggest that AD develops and exhibit the symptoms at 40 years of age [35,36].…”

Section: Causes Of Alzheimer's Diseasementioning

confidence: 99%

A Current Understanding of Alzheimers Disease and the Prospects of Phytopharmacological Intervention as a Management Strategy

Kk¹

2015

J Neurol Disord

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Brain cholinesterases: II. The molecular and cellular basis of Alzheimer's disease

Cited by 52 publications

References 87 publications

Amyloid beta: structure, biology and structure-based therapeutic development

Amyloid beta: structure, biology and structure-based therapeutic development

In vitro Anticholinesterase Activity of Various Alkaloids

A Current Understanding of Alzheimers Disease and the Prospects of Phytopharmacological Intervention as a Management Strategy

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