Inhibition of acetylcholinesterase in CSF versus brain assessed by 11C-PMP PET in AD patients treated with galantamine

Darreh‐Shori, Taher; Kadir, Ahmadul; Almkvist, Ove; Grut, Michaela; Wall, Anders; Blomquist, Gunnar; Eriksson, Bo; Långström, Bengt; Nordberg, Agneta

doi:10.1016/j.neurobiolaging.2006.09.020

Cited by 60 publications

(68 citation statements)

References 70 publications

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“…Secondly, upregulation of nAChRs may be dependent on dose and duration of treatment. The dose used in the current study (16 mg) causes significant AChE inhibition (approximately 30%, Darreh-Shori et al 2008), and, in a recent study in which 30-40% inhibition of cortical AChE was reported, a higher dose of galantamine (24 mg) also failed to increase [ 11 C]-nicotine binding . Furthermore, treatment dose and duration was sufficient to observe significant cognitive changes in this cohort.…”

Section: Discussionmentioning

confidence: 51%

Galantamine-induced improvements in cognitive function are not related to alterations in α4β2 nicotinic receptors in early Alzheimer’s disease as measured in vivo by 2-[18F]Fluoro-A-85380 PET

et al. 2008

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Performance on global measures of cognition significantly improved following galantamine treatment (p < 0.05). This improvement extended to specific cognitive measures of language and verbal learning. No significant differences in nAChR DV(S) before and after galantamine treatment were found. The treatment-induced improvement in cognition was not correlated with regional or global nAChR DV(S), suggesting that changes in nAChRs may not be responsible for the improvements in cognition following galantamine in patients with mild AD.

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Section: Discussionmentioning

confidence: 51%

Galantamine-induced improvements in cognitive function are not related to alterations in α4β2 nicotinic receptors in early Alzheimer’s disease as measured in vivo by 2-[18F]Fluoro-A-85380 PET

et al. 2008

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“…Initially, treatment with ChEIs increases the synaptic level of ACh (Giacobini et al 1996) and hence the AChE activity in the stimulated cortical neurons (Darreh-Shori et al 2002, 2006b. The increased AChE activity in turn reduces the ACh levels, which are counterbalanced by an increase in cortical 11 Cnicotine binding (low k 2 *) to compensate for the lowered ACh level in the synaptic cleft.…”

Section: Discussionmentioning

confidence: 99%

Changes in brain 11C–nicotine binding sites in patients with mild Alzheimer’s disease following rivastigmine treatment as assessed by PET

et al. 2007

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“…Even though previous studies on CSF cholinergic markers obtained conflicting data (119,120), recent reports have demonstrated alterations in the molecular forms and glycosylation patterns of acetylcholinesterase (AChE) in the CSF of AD patients, which reflect changes in the brain and might be useful as a marker of AD progression (121). It has been hypothesized that different AChE species and variants differ in their responses to disease and their interactions with Aβ and abnormally hyperphosphorylated tau.…”

Section: Novel Csf Biomarkersmentioning

confidence: 99%

Update on the core and developing cerebrospinal fluid biomarkers for Alzheimer disease

et al. 2014

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Alzheimer disease (AD) is a complex neurodegenerative disorder, whose prevalence will dramatically rise by 2050. Despite numerous clinical trials investigating this disease, there is still no effective treatment. Many trials showed negative or inconclusive results, possibly because they recruited only patients with severe disease, who had not undergone disease-modifying therapies in preclinical stages of AD before severe degeneration occurred. Detection of AD in asymptomatic at risk individuals (and a few presymptomatic individuals who carry an autosomal dominant monogenic AD mutation) remains impractical in many of clinical situations and is possible only with reliable biomarkers. In addition to early diagnosis of AD, biomarkers should serve for monitoring disease progression and response to therapy. To date, the most promising biomarkers are cerebrospinal fluid (CSF) and neuroimaging biomarkers. Core CSF biomarkers (amyloid β1-42, total tau, and phosphorylated tau) showed a high diagnostic accuracy but were still unreliable for preclinical detection of AD. Hence, there is an urgent need for detection and validation of novel CSF biomarkers that would enable early diagnosis of AD in asymptomatic individuals. This article reviews recent research advances on biomarkers for AD, focusing mainly on the CSF biomarkers. In addition to core CSF biomarkers, the potential usefulness of novel CSF biomarkers is discussed.

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Inhibition of acetylcholinesterase in CSF versus brain assessed by 11C-PMP PET in AD patients treated with galantamine

Cited by 60 publications

References 70 publications

Galantamine-induced improvements in cognitive function are not related to alterations in α4β2 nicotinic receptors in early Alzheimer’s disease as measured in vivo by 2-[18F]Fluoro-A-85380 PET

Galantamine-induced improvements in cognitive function are not related to alterations in α4β2 nicotinic receptors in early Alzheimer’s disease as measured in vivo by 2-[18F]Fluoro-A-85380 PET

Changes in brain 11C–nicotine binding sites in patients with mild Alzheimer’s disease following rivastigmine treatment as assessed by PET

Update on the core and developing cerebrospinal fluid biomarkers for Alzheimer disease

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