Human plasma semicarbazide sensitive amine oxidase (SSAO), β-amyloid protein and aging

Hernandez, Maria; Esteban, Miriam; Szabo, Paul; Boada, Merçé; Unzeta, Mercedes

doi:10.1016/j.neulet.2005.04.074

Cited by 65 publications

(26 citation statements)

References 26 publications

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“…For example, a formaldehyde generating enzyme, semicarbazide-sensitive amine oxidase (SSAO), SSAO activity is increased in human plasma during aging37, and associated with formaldehyde accumulation38. A specific formaldehyde degrading enzyme39, ADH3 (FDH), its activity is decreased in human during aging40.…”

Section: Discussionmentioning

confidence: 99%

Aging-associated excess formaldehyde leads to spatial memory deficits

Tong

Han

Luo

et al. 2013

Sci Rep

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Recent studies show that formaldehyde participates in DNA demethylation/methylation cycle. Emerging evidence identifies that neuronal activity induces global DNA demethylation and re-methylation; and DNA methylation is a critical step for memory formation. These data suggest that endogenous formaldehyde may intrinsically link learning-responsive DNA methylation status and memory formation. Here, we report that during spatial memory formation process, spatial training induces an initial global DNA demethylation and subsequent re-methylation associated with hippocampal formaldehyde elevation then decline to baseline level in Sprague Dawley rats. Scavenging this elevated formaldehyde by formaldehyde-degrading enzyme (FDH), or enhancing DNA demethylation by a DNA demethylating agent, both led to spatial memory deficits by blocking DNA re-methylation in rats. Furthermore, we found that the normal adult rats intrahippocampally injected with excess formaldehyde can imitate the aged-related spatial memory deficits and global DNA methylation decline. These findings indicate that aging-associated excess formaldheyde contributes to cognitive decline during aging.

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Section: Discussionmentioning

confidence: 99%

Aging-associated excess formaldehyde leads to spatial memory deficits

Tong

Han

Luo

et al. 2013

Sci Rep

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“…4) Mutations of formaldehyde metabolismrelated genes. Activities of semicarbazide-sensitive amine oxidase (SSAO, a blood formaldehyde-generating enzyme) are elevated in aged rats, as well as in patients suffering from AD [41][42][43]. Knockout of ALDH2 (a formaldehyde-degrading enzyme) induces memory loss and neurodegenerative disease [44].…”

Section: Exogenous and Endogenous Factors Induce Formaldehyde Accumulmentioning

confidence: 99%

Urine Formaldehyde: A Non-Invasive Marker for Alzheimer’s Disease?

Tong¹

2017

J Alzheimers Dis Parkinsonism

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“…SSAO/VAP-1 metabolizes only primary amines producing aldehydes, hydrogen peroxide and ammonia, which are able to induce oxidative stress and cellular damage when overproduced (Yu and Deng, 1998). SSAO/VAP-1 is localized at the cell membrane and is released into blood as soluble form that is altered in several human pathologies (Kurkijärvi et al, 1998; Boomsma et al, 2003), including AD (Ferrer et al, 2002; del Mar Hernandez et al, 2005) and cerebral ischemia (Airas et al, 2008). The mediators that induce these alterations in the SSAO/VAP-1 levels are still unknown, but it is believed that increased SSAO/VAP-1 levels may contribute to the physiopathology of these diseases, thus constituting a potential therapeutic target (Conklin et al, 1998; Solé et al, 2008).…”

Section: Diseases Without Current Monoaminergic Treatmentsmentioning

confidence: 99%

Monoaminergic and Histaminergic Strategies and Treatments in Brain Diseases

et al. 2016

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The monoaminergic systems are the target of several drugs for the treatment of mood, motor and cognitive disorders as well as neurological conditions. In most cases, advances have occurred through serendipity, except for Parkinson's disease where the pathophysiology led almost immediately to the introduction of dopamine restoring agents. Extensive neuropharmacological studies first showed that the primary target of antipsychotics, antidepressants, and anxiolytic drugs were specific components of the monoaminergic systems. Later, some dramatic side effects associated with older medicines were shown to disappear with new chemical compounds targeting the origin of the therapeutic benefit more specifically. The increased knowledge regarding the function and interaction of the monoaminergic systems in the brain resulting from in vivo neurochemical and neurophysiological studies indicated new monoaminergic targets that could achieve the efficacy of the older medicines with fewer side-effects. Yet, this accumulated knowledge regarding monoamines did not produce valuable strategies for diseases where no monoaminergic drug has been shown to be effective. Here, we emphasize the new therapeutic and monoaminergic-based strategies for the treatment of psychiatric diseases. We will consider three main groups of diseases, based on the evidence of monoamines involvement (schizophrenia, depression, obesity), the identification of monoamines in the diseases processes (Parkinson's disease, addiction) and the prospect of the involvement of monoaminergic mechanisms (epilepsy, Alzheimer's disease, stroke). In most cases, the clinically available monoaminergic drugs induce widespread modifications of amine tone or excitability through neurobiological networks and exemplify the overlap between therapeutic approaches to psychiatric and neurological conditions. More recent developments that have resulted in improved drug specificity and responses will be discussed in this review.

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Human plasma semicarbazide sensitive amine oxidase (SSAO), β-amyloid protein and aging

Cited by 65 publications

References 26 publications

Aging-associated excess formaldehyde leads to spatial memory deficits

Aging-associated excess formaldehyde leads to spatial memory deficits

Urine Formaldehyde: A Non-Invasive Marker for Alzheimer’s Disease?

Monoaminergic and Histaminergic Strategies and Treatments in Brain Diseases

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