No evidence for abnormalities in kinetics of platelet monoamine oxidase in Alzheimer's disease

Ch, Konings; Scheltens, Philip; Kuiper, Michael; Ec, Wolters

doi:10.1016/0009-8981(95)06130-4

Cited by 4 publications

(4 citation statements)

References 12 publications

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“…These AD-related findings were subsequently confirmed in at least 12 clinical studies from different research groups [57, 59, 73, 112–120]. Five other studies, however, reported no AD-related activity increase [58, 61, 73, 99, 121]. Importantly, instead of phenethylamine, three of these studies used the substrates tyramine or kynuramine [61, 73, 99], both converted by Mao-A and Mao-B [122].…”

Section: Reviewmentioning

confidence: 64%

“…Five other studies, however, reported no AD-related activity increase [58, 61, 73, 99, 121]. Importantly, instead of phenethylamine, three of these studies used the substrates tyramine or kynuramine [61, 73, 99], both converted by Mao-A and Mao-B [122]. In a recent study, Mao-B activity quantified by kynuramine has been found to be significantly lower in late stage AD patients as compared to healthy controls, whereas in early and middle stage AD Mao-B activity was not changed significantly [99].…”

Section: Reviewmentioning

confidence: 99%

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Platelets, a reliable source for peripheral Alzheimer’s disease biomarkers?

Veitinger

Varga

Guterres

et al. 2014

acta neuropathol commun

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Peripheral biomarkers play an indispensable role in quick and reliable diagnoses of any kind of disease. With the population ageing, the number of people suffering from age-related diseases is expected to rise dramatically over the coming decades. In particular, all types of cognitive deficits, such as Alzheimer’s disease, will increase. Alzheimer’s disease is characterised mainly by coexistence of amyloid plaques and neurofibrillary tangles in brain. Reliable identification of such molecular characteristics antemortem, however, is problematic due to restricted availability of appropriate sample material and definitive diagnosis is only possible postmortem. Currently, the best molecular biomarkers available for antemortem diagnosis originate from cerebrospinal fluid. Though, this is not convenient for routine diagnosis because of the required invasive lumbar puncture. As a consequence, there is a growing demand for additional peripheral biomarkers in a more readily accessible sample material. Blood platelets, due to shared biochemical properties with neurons, can constitute an attractive alternative as discussed here. This review summarises potential platelet Alzheimer’s disease biomarkers, their role, implication, and alteration in the disease. For easy comparison of their performance, the Hedge effect size was calculated whenever data were available.

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Section: Reviewmentioning

confidence: 64%

Section: Reviewmentioning

confidence: 99%

Platelets, a reliable source for peripheral Alzheimer’s disease biomarkers?

Veitinger

Varga

Guterres

et al. 2014

acta neuropathol commun

View full text Add to dashboard Cite

show abstract

“…However, several studies have indicated that MAO activity in platelets is not associated with the pathogenesis of AD (67)(68)(69). The MMSE indicated that no correlation was present between platelet MAO-B activity and the cognitive score in patients with AD (54).…”

Section: Increased Mao Activity In the Platelets Of Patients With Ad?mentioning

confidence: 99%

Monoamine oxidase inhibitors: Promising therapeutic agents for Alzheimer’s disease (Review)

Cai

2014

Molecular Medicine Reports

165

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Abstract. Activated monoamine oxidase (MAO) has a critical role in the pathogenesis of Alzheimer's disease (AD), including the formation of amyloid plaques from amyloid β peptide (Aβ) production and accumulation, formation of neurofibrillary tangles, and cognitive impairment via the destruction of cholinergic neurons and disorder of the cholinergic system. Several studies have indicated that MAO inhibitors improve cognitive deficits and reverse Aβ pathology by modulating proteolytic cleavage of amyloid precursor protein and decreasing Aβ protein fragments. Thus, MAO inhibitors may be considered as promising therapeutic agents for AD.

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“…Monoamino-oxidase-B (MAO-B) is an important enzyme located in the mitochondria and plays a role in metabolic processes of serotonin. Studies on platelet MAO-B activity yielded inconsistent results up to date: increased MAO-B activity was reported by several groups [116][117][118][119][120][121][122][123][124][125][126], while few researchers could not find any abnormalities [127,128]. The decline of mini-mental state examination scores (MMSE) preceded the elevation of MAO-B activity [116][117][118][119].…”

Section: Monoamino-oxidase Bmentioning

confidence: 99%