Blood markers in Alzheimer disease: Subnormal acetylcholinesterase and butyrylcholinesterase in lymphocytes and erythrocytes

Inestrosa, Nibaldo C.; Alarcón, Rodrigo; Arriagada, Jorge R.; Donoso, Archibaldo; Álvarez, Jaime; Campos, Eliseo O.

doi:10.1016/0022-510x(94)90044-2

Cited by 37 publications

(16 citation statements)

References 26 publications

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“…By contrast, there is no change in TH, ChAT, and AChE immunoreactivity in the PBL of AD subjects compared with controls. This last finding is in contrast to the results of a previous study which reported a decrease in AChE activity in the lymphocytes of AD subjects [16]. Several factors may account for this discrepancy, including the different methodologies used and the characteristics of AD subjects included.…”

Section: Discussioncontrasting

confidence: 56%

Increased Lymphocyte Dopamine β-Hydroxylase Immunoreactivity in Alzheimer’s Disease: Compensatory Response to Cholinergic Deficit?

Giubilei

Calderaro

Antonini

et al. 2004

Dement Geriatr Cogn Disord

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There is growing interest in the characterization of peripheral blood lymphocytes (PBL) as a biological tool with which to investigate changes in the neurotransmitter-receptor system in neurodegenerative disorders. Here we show a slight decrease in acetylcholinesterase (AChE) and a significant increase in dopamine β-hydroxylase (DBH) immunoreactivity in the PBL of patients with probable Alzheimer’s disease (AD). Therapy with AChE inhibitors completely reversed the increase in DBH immunoreactivity. We hypothesize that the increase in DBH immunoreactivity may represent a compensatory response to cholinergic impairment. Our findings suggest that neurochemical interactions between the noradrenergic and cholinergic systems may be measured at a peripheral level in AD.

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Section: Discussioncontrasting

confidence: 56%

Increased Lymphocyte Dopamine β-Hydroxylase Immunoreactivity in Alzheimer’s Disease: Compensatory Response to Cholinergic Deficit?

Giubilei

Calderaro

Antonini

et al. 2004

Dement Geriatr Cogn Disord

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“…In fact, AChE had little effect on the aggregation of the highly amyloidogenic Dutch variant (Inestrosa et al, 1996). However, when the Aβ val118 → Ala was incubated with AChE, a significant increase in the amyloid fibrils was observed (Inestrosa et al, 1996; Inestrosa and Alarcon, 1998). Previous investigations have shown that wild-type Aβ 1 → 40 is able to bind AChE, while the Dutch variant Aβ Glu22 → Gln is not (Muñoz and Inestrosa, 1999).…”

Section: Is There a Role For Ache In The Pathogenesis Of Neurodegenermentioning

confidence: 99%

Interactions of AChE with A? Aggregates in Alzheimer?s Brain: Therapeutic Relevance of IDN 5706

Carvajal¹,

Inestrosa²

2011

Front. Mol. Neurosci.

145

101

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Acetylcholinesterase (AChE; EC 3.1.1.7) plays a crucial role in the rapid hydrolysis of the neurotransmitter acetylcholine, in the central and peripheral nervous system and might also participate in non-cholinergic mechanism related to neurodegenerative diseases. Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by a progressive deterioration of cognitive abilities, amyloid-β (Aβ) peptide accumulation and synaptic alterations. We have previously shown that AChE is able to accelerate the Aβ peptide assembly into Alzheimer-type aggregates increasing its neurotoxicity. Furthermore, AChE activity is altered in brain and blood of Alzheimer’s patients. The enzyme associated to amyloid plaques changes its enzymatic and pharmacological properties, as well as, increases its resistant to low pH, inhibitors and excess of substrate. Here, we reviewed the effects of IDN 5706, a hyperforin derivative that has potential preventive effects on the development of AD. Our results show that treatment with IDN 5706 for 10 weeks increases brain AChE activity in 7-month-old double transgenic mice (APPSWE–PS1) and decreases the content of AChE associated with different types of amyloid plaques in this Alzheimer’s model. We concluded that early treatment with IDN 5706 decreases AChE–Aβ interaction and this effect might be of therapeutic interest in the treatment of AD.

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“…[46][47][48] Recent studies suggest that Ach is synthesized by lymphocytes and released from activated T-cells into the vicinity of Ach receptors of target cells, interacting with the receptors before hydrolysis by AchE. [49][50][51][52] In consideration of the fact that several studies have suggested that immune interactions between the central nervous system and peripheral blood cells of AD patients exist, 53 we are hypothesizing that AchE inhibitor (AchEI) treatment may interact with the cytokine network modulating the cytokine cycles possibly involved in the pathogenic mechanism for neurodegeneration in AD. AchEI may possibly contribute in delaying the disease progression interfering in the delicate balance of the cytokine cascade.…”

mentioning

confidence: 99%

Alzheimer Patients Treated With an AchE Inhibitor Show Higher IL-4 and Lower IL-1β Levels and Expression in Peripheral Blood Mononuclear Cells

Gambi

Reale²,

Iarlori³

et al. 2004

Journal of Clinical Psychopharmacology

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The study evaluates the expression and production of cytokines in peripheral blood mononuclear cells of patients with Alzheimer disease treated or not treated with acetylcholinesterase inhibitor, which enhances neuronal transmission. Cytokines associated with brain inflammation such as interleukin (IL)-1beta, IL-6, and tumor necrosis factor-alpha have been implicated in the regulation of amyloid peptide protein synthesis. The anti-inflammatory cytokine, IL-4, may suppress the activity of IL-1beta. Patients were assessed for clinical and immunologic features at baseline and after 1 month of treatment with Donepezil, an acetylcholinesterase inhibitor. Peripheral blood mononuclear cells were cultured with and without phytohemagglutinin stimulation. IL-1beta and IL-4 levels were measured by enzyme-linked immunosorbent assay. Reverse transcriptase-polymerase chain reaction was used to determine the expression of cytokines in peripheral mononuclear cells. Compared with untreated patients and healthy control subjects, IL-1beta levels and expression decreased in Alzheimer disease patients treated with Donepezil (P < 0.001). In contrast, IL-4 levels and expression were significantly higher in Alzheimer patients treated with the acetylcholinesterase inhibitor. This increment was observed in both unstimulated and phytohemagglutinin-stimulated peripheral blood mononuclear cells.

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Blood markers in Alzheimer disease: Subnormal acetylcholinesterase and butyrylcholinesterase in lymphocytes and erythrocytes

Cited by 37 publications

References 26 publications

Increased Lymphocyte Dopamine β-Hydroxylase Immunoreactivity in Alzheimer’s Disease: Compensatory Response to Cholinergic Deficit?

Increased Lymphocyte Dopamine β-Hydroxylase Immunoreactivity in Alzheimer’s Disease: Compensatory Response to Cholinergic Deficit?

Interactions of AChE with A? Aggregates in Alzheimer?s Brain: Therapeutic Relevance of IDN 5706

Alzheimer Patients Treated With an AchE Inhibitor Show Higher IL-4 and Lower IL-1β Levels and Expression in Peripheral Blood Mononuclear Cells

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