C-reactive protein: A pentraxin with anti-acetylcholine activity

Nazarov, Peter G.; Крылова, И. Б.; Евдокимова, Н. Р.; Nezhinskaya, G. I.; Butyugov, Alexander A.

doi:10.1016/j.lfs.2007.04.031

Cited by 16 publications

(14 citation statements)

References 12 publications

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“…Various cytokines such as tumor necrosis factor, C-reactive protein (CRP) and interleukin-6 or inflammatory substances in peripheral tissue and inflammation-related substances in the central nervous system are induced during inflammation [28], and some of these have anticholinergic properties. In fact, Nazarov et al [29] reported that CRP, which increases during inflammatory states, may result in AA by capturing ACh or binding to the ACh receptor, whereas Tsuruta et al [30] reported that plasma AA was related to CRP in critically ill and injured patients. Furthermore, Horiuchi et al [31] reported that an endogenous immunologically active peptide (apelin) inhibited cholinergic activity by binding to the ACh receptor, and Jadcherla [32] found that inflammation inhibited muscarinic receptormediated signaling.…”

Section: Discussionmentioning

confidence: 99%

Donepezil Abolishes Anticholinergic Activity in a Patient with Amnesia

et al. 2013

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We report the case of a 74-year-old woman who presented with amnesia and positive serum anticholinergic activity (SAA), which disappeared after treatment with the cholinesterase inhibitor donepezil for 1 year. Her only other regular medications were topical glaucoma preparations. We suggest that mental stress, mild cognitive impairment and Alzheimer’s disease pathology combined to generate SAA in this patient. We also consider that SAA may have subsequently become negative because of upregulation of acetylcholine production by donepezil, and because the patient’s other medications and physical condition (including glaucoma) remained unchanged during the 1-year period.

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Section: Discussionmentioning

confidence: 99%

Donepezil Abolishes Anticholinergic Activity in a Patient with Amnesia

et al. 2013

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“…NMDAR expression is also upregulated in central nervous system disorders, leading to hyperactivity of the inflammatory system [4]. Cytokines that have anticholinergic activity (AA) may appear as a result of this inflammation [5]. Therefore, we previously hypothesized that both AA in the central nervous system and peripheral tissue (serum anticholinergic activity, SAA) may appear endogenously in the moderate stage of AD [6].…”

Section: Introductionmentioning

confidence: 99%

Pharmacotherapy for Neurocognitive Disorders Based on the Hypothesis of Endogenous Appearance of Anticholinergic Activity

et al. 2015

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We previously proposed the hypothesis of endogenous anticholinergic activity (AA) in Alzheimer's disease (AD). According to this hypothesis, the downregulation of acetylcholine seen in AD is associated with upregulation/hyperactivity of N-methyl-D-aspartate receptor (NMDAR). The hyperactivation of NMDAR then induces inflammation, which, in turn, causes AA to appear endogenously. Based on this hypothesis, we commented that cholinesterase inhibitors (ChEIs) are ‘preventative' therapy for AD and NMDAR antagonists are the true ‘treatment' for AD. We also noted that ChEIs, such as donepezil, could treat delirium. Moreover, we proposed measuring serum anticholinergic activity in patients, particularly AD patients, in out-of-hospital pharmacies to monitor the anticholinergic burden for targeted treatment.

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“…The downregulation of ACh is related to cognitive dysfunctions such as memory disturbance and disorientations [3,7]. However, it is considered that ACh also regulates inflammatory system, i. e., referred to as antiinflammatory pathway [8,9]. Therefore, we speculated that some cytokines caused by upregulations of inflammations have anticholinergic activity (AA), which accelerated AD pathology (amyloids and tau) [10][11][12].…”

Section: Discussionmentioning

confidence: 99%

Rivastigimine for Relatively Younger Alzheimer’s Disease Patient

Horiuchi¹,

Hori

Hosoi³

et al. 2014

rain Disord Ther

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We presented the patient with relative younger Alzheimer's disease (AD) whose clinical symptoms and cognitive functions were responsive not to donepezil but to rivastigmine. Age of initial visit our memory clinic of this patient was relatively younger. It is considered that in relative older patient both AD pathology and aging cause cognitive dysfunctions. However, in relative younger patient not aging but only AD pathology causes cognitive dysfunctions. Therefore, AD pathology was thought to be more pronounced in our patient than relatively older patients with same cognitive disturbances. In AD, glia cells and amyloids proliferate and nervous cells shrink. Butyrylcholinesterase (BuChE) exists in glia cells and amyloids. Therefore, when AD progresses, acetylcholinesterase (AChE) decreases and BuChE increases. Accordingly the ratio of BuChE/AChE increases. Therefore, when at mild stage such our patient, not donepezil but rivastigmine which has inhibiting actions on both AChE and BuChE was suitable.

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C-reactive protein: A pentraxin with anti-acetylcholine activity

Cited by 16 publications

References 12 publications

Donepezil Abolishes Anticholinergic Activity in a Patient with Amnesia

Donepezil Abolishes Anticholinergic Activity in a Patient with Amnesia

Pharmacotherapy for Neurocognitive Disorders Based on the Hypothesis of Endogenous Appearance of Anticholinergic Activity

Rivastigimine for Relatively Younger Alzheimer’s Disease Patient

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