Platelet MAO-B activity as a marker of behavioural characteristics in dementia disorders

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

“…This was demonstrated by [ 11 C]-L-deprenyl using whole hemisphere autoradiography (38)(39)(40), epidemiology (41,42), morphology (43), as well as single-photon emission computed tomography (44). Such studies demonstrated that: i) MAO activity in platelets was significantly increased in patients with AD and acted as a marker of behavioral characteristics in dementia disorders (41,(45)(46)(47)(48); ii) there were early and persistent alterations in MAO-A and -B in the brains of patients with AD (49); iii) activated MAO led to cognitive dysfunction (50); iv) activated MAO destroyed cholinergic neurons and caused disorders of the cholinergic system (51); v) activated MAO contributed to the formation of amyloid plaques (13,14) and vi) activated MAO was associated with the formation of NFTs.…”

“…Studies on the association between platelet MAO-B activity, clinical features and cerebrospinal fluid (CSF) monoamine metabolites have demonstrated the importance of MAO-B activity in platelets as a biological marker of AD (47,66). An increased activity of this enzyme may constitute a marker for vulnerability towards behavioral disturbance (47).…”

“…An increased activity of this enzyme may constitute a marker for vulnerability towards behavioral disturbance (47). According to a Mini Mental State Examination (MMSE) of three groups with 23 patients in the early (MMSE score of [19][20][21][22][23][24], 23 patients in the middle (MMSE score of 10-18) and 28 patients in the late (MMSE score of 0-9) phases of AD, as well as 49 age-matched healthy females, significant correlations between MMSE scores and MAO-B activity and age were identified, suggesting that these markers may indicate the severity and/or clinical progress of AD (42,45).…”

Recent Developments in the Regulation of Monoamine Oxidase Form and Function: Is the Current Model Restricting Our Understanding of the Breadth of Contribution of Monoamine Oxidase to Brain [dys]Function?

“…For example, AD-related pathology is thought to rely primarily on the MAO-B isoform [88,89] since MAO-B activity and MAO-B mRNA have been reported to be increased in platelets of AD patients [90,91], as well as in the hippocampus, thalamus, and cerebral cortex, which are regions that undergo extensive neuronal cell death during AD [92,93]. The MAO-B increase could be due to the local infiltration of glial cells in these areas as MAO-B is mainly expressed in this cell type, a significant proportion of which are found in the proximity of -amyloid plaques (a hallmark of AD pathology) [32,88,94].…”

Comparative platelet proteome analysis reveals an increase of monoamine oxidase-B protein expression in Alzheimer's disease but not in non-demented Parkinson's disease patients

“…In addition, numerous studies reported an increase of monoamine oxidase-B (Mao-B) enzymatic activity in both brain tissue and platelets of AD [7,8] or PD [9] patients that was stronger than that observed during healthy ageing [10,11]. It is attractive to speculate that many of these modifications might be reflected in the platelet proteome.…”