Decreased Cerebrospinal Fluid Acetylcholinesterase in Patients with Subcortical Ischemic Vascular Dementia

Wallin, Anders; Sjögren, Magnus; Blennow, Kaj; Davidsson, Pia

doi:10.1159/000072803

Cited by 45 publications

(40 citation statements)

References 64 publications

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“…Postmortem examinations have revealed significant reductions in ChAT activity in the hippocampus and temporal cortex of VaD patients [23,24] . Tohgi et al and Wallin et al observed significantly reduced CSF ACh concentrations in patients with Binswanger or multiinfarct dementia (MID) [25,26] . These results are consistent with the finding that the number of cholinergic neurons in the nucleus basalis of Meynert is reduced in MID [27] .…”

Section: Cholinergic Deficiency In Vad Animal Models and Vad Patientsmentioning

confidence: 99%

Cholinergic deficiency involved in vascular dementia: possible mechanism and strategy of treatment

2009

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Vascular dementia (VaD) is a progressive neurodegenerative disease with a high prevalence. Several studies have recently reported that VaD patients present cholinergic deficits in the brain and cerebrospinal fluid (CSF) that may be closely related to the pathophysiology of cognitive impairment. Moreover, cholinergic therapies have shown promising effects on cognitive improvement in VaD patients. The precise mechanisms of these cholinergic agents are currently not fully understood; however, accumulating evidence indicates that these drugs may act through the cholinergic anti-inflammatory pathway, in which the efferent vagus nerve signals suppress pro-inflammatory cytokine release and inhibit inflammation, although regulation of oxidative stress and energy metabolism, alleviation of apoptosis may also be involved. In this paper, we provide a brief overview of the cholinergic treatment strategy for VaD and its relevant mechanisms of anti-inflammation.

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Section: Cholinergic Deficiency In Vad Animal Models and Vad Patientsmentioning

confidence: 99%

Cholinergic deficiency involved in vascular dementia: possible mechanism and strategy of treatment

2009

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“…61 The 20 largest studies 14,20,24,41,50,56,[62][63][64][65][66][67][68][69][70][71][72][73][74][75] including more than 2000 AD patients and 1000 controls, evaluating the most commonly used ELISA method for T-tau in CSF, 14 are summarized in Table 2. The mean sensitivity to discriminate AD from nondemented aged individuals has been 81%, at a specificity level of 91% (Table 2).…”

Section: Csf T-taumentioning

confidence: 99%

Cerebrospinal fluid protein biomarkers for Alzheimer’s disease

2004

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Summary:The introduction of acetylcholine esterase (AChE) inhibitors as a symptomatic treatment of Alzheimer's disease (AD) has made patients seek medical advice at an earlier stage of the disease. This has highlighted the importance of diagnostic markers for early AD. However, there is no clinical method to determine which of the patients with mild cognitive impairment (MCI) will progress to AD with dementia, and which have a benign form of MCI without progression. In this paper, the performance of cerebrospinal fluid (CSF) protein biomarkers for AD is reviewed. The diagnostic performance of the three biomarkers, total tau, phospho-tau, and the 42 amino acid form of ␤-amyloid have been evaluated in numerous studies and their ability to identify incipient AD in MCI cases has also been studied. Some candidate AD biomarkers including ubiquitin, neurofilament proteins, growth-associated protein 43 (neuromodulin), and neuronal thread protein (AD7c) show interesting results but have been less extensively studied. It is concluded that CSF biomarkers may have clinical utility in the differentiation between AD and several important differential diagnoses, including normal aging, depression, alcohol dementia, and Parkinson's disease, and also in the identification of Creutzfeldt-Jakob disease in cases with rapidly progressive dementia. Early diagnosis of AD is not only of importance to be able to initiate symptomatic treatment with AChE inhibitors, but will be the basis for initiation of treatment with drugs aimed at slowing down or arresting the degenerative process, such as ␥-secretase inhibitors, if these prove to affect AD pathology and to have a clinical effect.

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“…First, both cholinergic neuronal deficits (Keverne et al, 2007) and cholinergic denervation (Mesulam et al, 2003) have been identified in patients with cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), a purely genetic form of vascular dementia (VaD). Secondly, significantly decreased cerebrospinal fluid acetylcholine concentrations were observed in patients with Binswanger or multi-infarct dementia (Tohgi et al, 1996;Wallin et al, 2003). Finally, clinical trials have prompted potential beneficial effects of cholinergic drugs in patients with VaD (Erkinjuntti et al, 2002;Black et al, 2003;Wilkinson et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

P4‐221: White Matter Damage in Cholinergic System Contributes to Cognitive Impairment in Subcortical Vascular Cognitive Impairment No Dementia

Liu

Zhu

Teipel

et al. 2016

Alzheimer's & Dementia

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Cholinergic deficiency has been implicated in the pathogenesis of vascular cognitive impairment (VCI), but the extent of involvement and underlying mechanism remain unclear. In this study, targeting the early stage of VCI, we determined regional atrophy within the basal forebrain and deficiency in cholinergic pathways in 25 patients with vascular cognitive impairment no dementia (VCIND) compared to 24 healthy elderly subjects. By applying stereotaxic cytoarchitectonic maps of the nucleus basalis of Meynert (NbM), no significant atrophy was identified in VCIND. Using probabilistic tractography analysis, our study tracked the two major white matter tracks which map to cholinergic pathways. We identified significantly lower fractional anisotropy (FA) in VCIND. Mediation analysis demonstrated that FA in the tracked pathways could fully account for the executive dysfunction, and partly mediate the memory and global cognition impairment. Our study suggests that the fibers mapped to the cholinergic pathways, but not the NbM, are significantly impaired in VCIND. MRI-based in vivo tracking of cholinergic pathways together with NbM measurement may become a valuable in vivo marker for evaluating the cholinergic system in cognitive disorders.

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Decreased Cerebrospinal Fluid Acetylcholinesterase in Patients with Subcortical Ischemic Vascular Dementia

Cited by 45 publications

References 64 publications

Cholinergic deficiency involved in vascular dementia: possible mechanism and strategy of treatment

Cholinergic deficiency involved in vascular dementia: possible mechanism and strategy of treatment

Cerebrospinal fluid protein biomarkers for Alzheimer’s disease

P4‐221: White Matter Damage in Cholinergic System Contributes to Cognitive Impairment in Subcortical Vascular Cognitive Impairment No Dementia

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