Cholinergic and glutamatergic alterations beginning at the early stages of Alzheimer disease: participation of the phospholipase A2 enzyme

Schaeffer, Evelin L.; Gattaz, Wagner F.

doi:10.1007/s00213-008-1092-0

Cited by 91 publications

(57 citation statements)

References 363 publications

(314 reference statements)

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“…In this study the Aβ (25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35) induce impairment in short term memory was significantly alleviated by the isorhamnetin treatment. It has been reported that Aβ induces the production of hydrogen peroxide and lipid peroxide in hippocampal neurons of the rat brain 28 .…”

Section: Effect Of Isorhamnetin On Aβ25-35 Induced Changes In Mrna Exmentioning

confidence: 67%

“…alone showed normal expressions of IL-β when compared with the control group. DISCUSSION: Aβ (25-35) is potential neurotoxic peptide for primary neuronal cortical cells which produces neurofibrillary tangles [25][26] and the toxicity induced by Aβ (25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35) in rodents resembles to AD which is suitable for the evaluation of Alzheimer's type of dementia. Isorhamnetin, which is an O-methylated metabolite formed in the small intestine and liver, and increased in the human brain, has a higher BBB permeability than aglycone by its apparent lipophilicity 27 .…”

Section: Effect Of Isorhamnetin On Aβ25-35 Induced Changes In Mrna Exmentioning

confidence: 99%

“…It is well accepted that oxidative stress (associated with MAO) contributes to the disturbance of neurotransmitters, including NE and the cholinergic system, which have a critical role in the cognitive impairment in AD [33][34][35] . Elevations in MAOA in Alzheimer neurons have been linked to increase in neurotoxic metabolites and neuronal loss.…”

Section: Effect Of Isorhamnetin On Aβ25-35 Induced Changes In Mrna Exmentioning

confidence: 99%

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Untitled

2016

IJPSR

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ABSTRACT:Oxidative stress appears to be an early event involved in the pathogenesis of Alzheimer's disease. The present study was designed to investigate the neuroprotective effects of isorhamnetin (IRN) against amyloid beta 25-35 (Aβ 25-35)-induced memory impairment and oxidative damage in rats. Memory task was assessed using Y-arm maze and it revealed the impairment in spatial memory. The IRN treated rats showed improvement in memory task. Aβ 25-35 induced animals also exhibited increase in hydrogen peroxide (H 2 O 2), Monoamine oxidase activity (MAO) and decrease in choline acetyltransferase (ChAT) activity. It also enhanced the expression of inducible nitric oxide synthase (iNOS) and proinflammatory cytokine, IL-β whereas all these abnormalities were reduced significantly in IRN treated rats showing the neuroprotective effect of IRN against Aβ 25-35 induced Alzheimer's disease (AD). Thus, IRN may be a potential therapeutic agent for Alzheimer's disease.

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Section: Effect Of Isorhamnetin On Aβ25-35 Induced Changes In Mrna Exmentioning

confidence: 67%

Section: Effect Of Isorhamnetin On Aβ25-35 Induced Changes In Mrna Exmentioning

confidence: 99%

Section: Effect Of Isorhamnetin On Aβ25-35 Induced Changes In Mrna Exmentioning

confidence: 99%

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2016

IJPSR

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“…In addition, secreted phospholipase A2 (PLA2) and other subtypes are highly expressed in platelets [41] , and play a critical role in the regulation of the inflammatory response [45] . PLA2 abnormalities have been consistently found in AD [46] , with important implications in membrane homeostasis and the inflammatory response. The involvement of platelet PLA2 in AD will be discussed in detail in a following section of this article.…”

Section: Inflamatory Factorsmentioning

confidence: 98%

Platelet biomarkers in Alzheimer’s disease

Talib

Joaquim²,

Forlenza³

2012

WJP

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The search for diagnostic and prognostic markers in Alzheimer's disease (AD) has been an area of active research in the last decades. Biochemical markers are correlates of intracerebral changes that can be identified in biological fluids, namely: peripheral blood (total blood, red and white blood cells, platelets, plasma and serum), saliva, urine and cerebrospinal fluid. An important feature of a biomarker is that it can be measured objectively and evaluated as (1) an indicator of disease mechanisms (markers of core pathogenic processes or the expression of downstream effects of these processes), or (2) biochemical responses to pharmacological or therapeutic intervention, which can be indicative of disease modification. Platelets have been used in neuropharmacological models since the mid-fifties, as they share several homeostatic functions with neurons, such as accumulation and release of neurotransmitters, responsiveness to variations in calcium concentration, and expression of membrane-bound compounds. Recent studies have shown that platelets also express several components related to the pathogenesis of AD, in particular to the amyloid cascade and the regulation of oxidative stress: thus they can be used in the search for biomarkers of the disease process. For instance, platelets are the most important source of circulating forms of the amyloid precursor protein and other important proteins such as Tau and glycogen synthase kinase-3B. Moreover, platelets express enzymes involved in membrane homeostasis (e.g., phospholipase A2), and markers of the inflammatory process and oxidative stress. In this review we summarize the available literature and discuss evidence concerning the potential use of platelet markers in AD.

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“…Although there are no reports on the direct association between MAO and the aforementioned neurotransmitter systems in AD, numerous studies suggest that activated MAO is indirectly involved in the close association between cognitive impairment and several neurotransmitter systems in AD (98-100). It is well accepted that oxidative stress (associated with MAO) contributes to the disturbance of aforementioned neurotransmitters, including NE and the cholinergic system, which have a critical role in the cognitive impairment in AD (100)(101)(102)(103). Considering that neuroinflammation is a key element in cognitive impairment and an intermediate for oxidative stress (104-107), MAO may act as a proinflammatory mediator, which causes cognitive impairment in AD.…”

Section: Mao Activation Contributes To Cognitive Impairment In Patienmentioning

confidence: 99%

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

Cai

2014

Molecular Medicine Reports

180

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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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Cholinergic and glutamatergic alterations beginning at the early stages of Alzheimer disease: participation of the phospholipase A2 enzyme

Abstract: Activation and inhibition of specific PLA(2) isoforms at different stages of AD could be of therapeutic importance and delay cognitive dysfunction and neurodegeneration.

Cited by 91 publications

References 363 publications

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Platelet biomarkers in Alzheimer’s disease

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

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