Platelet Monoamine Oxidase B Activity in Dementia

Abstract

Platelet monoamine oxidase B (MAO-B) activity has been found to increase significantly in demented patients. For the first time, a 4-year follow-up of platelet MAO-B activity and Mini-Mental State (MMS) was performed in patients with probable dementia of the Alzheimer type (DAT) and age-matched controls. MAO-B activity of DAT patients increased significantly 2 years after the beginning of the study as compared with controls and remained significantly higher for the entire period of the examinations (p < 0.0001). The decrease of the MMS scores did not correlate with the time course of the increase of platelet MAO-B activity (Spearman rank correlation test). The decline of the MMS scores of DAT patients preceded the elevation of MAO-B activity. Since degenerative processes in brain areas which are responsible for cognitive function and are reflected by the MMS scores rather affect cerebral cholinergic than monoaminergic neurotransmitter systems, degeneration of the latter at late stages of DAT might be reflected by increased platelet MAO-B activity.

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

“…However, Mao-B was stable increased from the early stage (SA = 1.20; effect size 2.7 n = 3), through the middle stage (SA = 1.22; effect size 1.36; n = 3) all the way to late stage (SA 1.18; effect size 1; n = 28) of our AD sample and did not correlate with MMSE of included AD patients. Hence, our observations were in accordance with earlier findings which similarly showed no correlation between the decrease of MMSE and an increase in the level of platelet Mao-B activity [68,69]. However, these observations indicate that the increase of Mao-B may be at an early stage of the disease, and cognitive decline may also be a consequence of the elevated expression and activity of this enzyme in the brain.…”

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.…”

Different effects of soluble and aggregated amyloid β42 on gene/protein expression and enzyme activity involved in insulin and APP pathways

“…Although we could find an inhibition of MAO-B activity after soluble peptide treatment, it cannot be concluded that these oligomers might be neuroprotective. An increased MAO-B activity was found in senile plaques (Saura et al, 1997) and in platelets of AD patients (Gotz et al, 1998), therefore our results of enhanced MAO-B activity following treatment with aggregated while not with soluble Aβ 42 peptides, might indicate the involvement of the fibrillar structures of Aβ 42 in the oxidative stress cascade known to play an important role in AD (Grünblatt et al, 2005;Grünblatt et al, 2010).…”

“…(Zhao et al, 2009). MAO-B activity is significantly increased in AD patients (Gotz et al, 1998;Grünblatt et al, 2005) and inhibition of MAO-B has a neuroprotective effects for AD (reviewed in (Riederer et al, 2004).…”