Collins D

References (7)

Title : Consistency of neuropsychiatric syndromes across dementias: results from the European Alzheimer Disease Consortium. Part II - Aalten_2008_Dement.Geriatr.Cogn.Disord_25_1
Author(s) : Aalten P , Verhey FR , Boziki M , Brugnolo A , Bullock R , Byrne EJ , Camus V , Caputo M , Collins D , De Deyn PP , Elina K , Frisoni G , Holmes C , Hurt C , Marriott A , Mecocci P , Nobili F , Ousset PJ , Reynish E , Salmon E , Tsolaki M , Vellas B , Robert PH
Ref : Dementia & Geriatric Cognitive Disorders , 25 :1 , 2008
Abstract : BACKGROUND/AIMS: The aim of this study was to determine the consistency of neuropsychiatric subsyndromes of the Neuropsychiatric Inventory across several clinical and demographic subgroups (e.g. dementia subtypes, dementia severity, medication use, age and gender) in a large sample of outpatients with dementia.
METHODS: Cross-sectional data of 2,808 patients with dementia from 12 centres from the European Alzheimer's Disease Consortium were collected. Principal component analysis was used for factor analysis. Subanalyses were performed for dementia subtypes, dementia severity, medication use, age and gender.
RESULTS: The results showed the relatively consistent presence of the 4 neuropsychiatric subsyndromes 'hyperactivity', 'psychosis', 'affective symptoms' and 'apathy' across the subanalyses. The factor structure was not dependent on dementia subtypes, age and gender but was dependent on dementia severity and cholinesterase use. The factors hyperactivity and affective symptoms were present in all subanalyses, but the presence of the factors apathy and psychosis was dependent on use of cholinesterase inhibitors and dementia severity, respectively. CONCLUSION: The present study provided evidence of the relative consistency of neuropsychiatric subsyndromes across dementia subtypes, age and gender, thereby stressing the importance of thinking about neuropsychiatric subsyndromes instead of separate symptoms. However, the subsyndromes apathy and psychosis were dependent on use of cholinesterase inhibitors and dementia severity.
ESTHER : Aalten_2008_Dement.Geriatr.Cogn.Disord_25_1
PubMedSearch : Aalten_2008_Dement.Geriatr.Cogn.Disord_25_1
PubMedID: 18025783

Title : Effect of acetylcholinesterase inhibitors on the binding of nicotinic alpha4beta2 receptor PET radiotracer, (18)F-nifene: A measure of acetylcholine competition - Easwaramoorthy_2007_Synapse_61_29
Author(s) : Easwaramoorthy B , Pichika R , Collins D , Potkin SG , Leslie FM , Mukherjee J
Ref : Synapse , 61 :29 , 2007
Abstract : Acetylcholinesterase inhibitors (AChEI's) are used to treat Alzheimer's disease (AD), and the putative mode of action is to increase acetylcholine (ACh) levels. Our goal is to evaluate competition of ACh with nicotinic alpha4beta2 receptor PET agonist radiotracer, 2-[(18)F]fluoro-3-[2-((S)-3-pyrrolinyl)methoxy]pyridine ((18)F-nifene). This ability to measure ACh-(18)F-nifene competition may have potential to assess efficacy of AChEI's in vivo. In vitro studies in rat brain slices used two AChEI's, physostigmine (PHY) and galanthamine (GAL). Brain slices were incubated with (18)F-nifene and various concentrations of PHY (0.2-20 microM) or GAL (0.4-4 microM) prior to (18)F-nifene treatment. For ACh competition, slices were also incubated with PHY + 100 nM ACh or GAL + 100 nM ACh or 100 nM ACh alone. Nonspecific binding of (18)F-nifene was determined using 300 microM nicotine. In the in vitro rat brain homogenate binding assay, ACh inhibited (3)H-cytisine binding to alpha4beta2 receptors with K(i) values of 19.2 nM (with PHY) and 34.7 microM (no PHY) indicating approximately 1.8 x 10(3) weaker binding of ACh in the absence of AChEI. Binding of (18)F-nifene was not affected by PHY (0.2-20 microM) or ACh 100 nM alone but decreased substantially by PHY + ACh 100 nM in all brain regions (down by >40% of control in thalamus). Similarly, for GAL (4 microM) no effect on (18)F-nifene binding occurred but GAL (0.4-4 microM) + ACh 100 nM showed a reduction of (18)F-nifene binding in all brain regions (down by approximately 15%). The reduction in both cases is a result of ACh competition with (18)F-nifene in the presence of AChEI. These preliminary in vitro results suggest that ACh is able to compete with (18)F-nifene at the alpha4beta2 receptors in the presence of PHY or GAL. The effect is AChEI-concentration dependent and is greater for PHY than GAL. Thus (18)F-nifene has promise for assessing ACh levels and AChEI effects in vivo.
ESTHER : Easwaramoorthy_2007_Synapse_61_29
PubMedSearch : Easwaramoorthy_2007_Synapse_61_29
PubMedID: 17068780

Title : Collaborative meta-analysis of individual participant data from observational studies of Lp-PLA2 and cardiovascular diseases - Ballantyne_2007_Eur.J.Cardiovasc.Prev.Rehabil_14_3
Author(s) : Ballantyne C , Cushman M , Psaty B , Furberg C , Khaw KT , Sandhu M , Oldgren J , Rossi GP , Maiolino G , Cesari M , Lenzini L , James SK , Rimm E , Collins R , Anderson J , Koenig W , Brenner H , Rothenbacher D , Berglund G , Persson M , Berger P , Brilakis E , McConnell JP , Sacco R , Elkind M , Talmud P , Cannon CP , Packard C , Barrett-Connor E , Hofman A , Kardys I , Witteman JC , Criqui M , Corsetti JP , Rainwater DL , Moss AJ , Robins S , Bloomfield H , Collins D , Wassertheil-Smoller S , Ridker P , Danesh J , Gu D , Nelson JJ , Thompson S , Zalewski A , Zariffa N , Di Angelantonio E , Kaptoge S , Thompson A , Walker M , Watson S , Wood A
Ref : Eur J Cardiovasc Prev Rehabil , 14 :3 , 2007
Abstract : BACKGROUND: A large number of observational epidemiological studies have reported generally positive associations between circulating mass and activity levels of lipoprotein-associated phospholipase A2 (Lp-PLA2) and the risk of cardiovascular diseases. Few studies have been large enough to provide reliable estimates in different circumstances, such as in different subgroups (e.g., by age group, sex, or smoking status) or at different Lp-PLA2 levels. Moreover, most published studies have related disease risk only to baseline values of Lp-PLA2 markers (which can lead to substantial underestimation of any risk relationships because of within-person variability over time) and have used different approaches to adjustment for possible confounding factors. OBJECTIVES: By combination of data from individual participants from all relevant observational studies in a systematic 'meta-analysis', with correction for regression dilution (using available data on serial measurements of Lp-PLA2), the Lp-PLA2 Studies Collaboration will aim to characterize more precisely than has previously been possible the strength and shape of the age and sex-specific associations of plasma Lp-PLA2 with coronary heart disease (and, where data are sufficient, with other vascular diseases, such as ischaemic stroke). It will also help to determine to what extent such associations are independent of possible confounding factors and to explore potential sources of heterogeneity among studies, such as those related to assay methods and study design. It is anticipated that the present collaboration will serve as a framework to investigate related questions on Lp-PLA2 and cardiovascular outcomes. METHODS: A central database is being established containing data on circulating Lp-PLA2 values, sex and other potential confounding factors, age at baseline Lp-PLA2 measurement, age at event or at last follow-up, major vascular morbidity and cause-specific mortality. Information about any repeat measurements of Lp-PLA2 and potential confounding factors has been sought to allow adjustment for possible confounding and correction for regression dilution. The analyses will involve age-specific regression models. Synthesis of the available observational studies of Lp-PLA2 will yield information on a total of about 15 000 cardiovascular disease endpoints.
ESTHER : Ballantyne_2007_Eur.J.Cardiovasc.Prev.Rehabil_14_3
PubMedSearch : Ballantyne_2007_Eur.J.Cardiovasc.Prev.Rehabil_14_3
PubMedID: 17301621
Gene_locus related to this paper: human-PLA2G7

Title : Non-dopaminergic treatment of cognitive impairment and dementia in Parkinson's disease: a review - Leroi_2006_J.Neurol.Sci_248_104
Author(s) : Leroi I , Collins D , Marsh L
Ref : Journal of Neurology Sci , 248 :104 , 2006
Abstract : OBJECTIVE: To review the clinical management of cognitive impairment and dementia related to Parkinson's disease (PD), with emphasis on pharmacologic intervention strategies such as cholinesterase inhibitors. DATA SOURCES: A MEDLINE, EMBASE, PsychINFO, and Cochrane Collaboration search of English language literature from 1970 to 2004 was performed to identify reviews, studies, case reports, and letters pertaining to the treatment of cognitive impairment in PD. The bibliographies of selected articles were reviewed for additional references. STUDY SELECTION: Human studies or case reports in adults with PD describing the use of drug and other therapies for the treatment of cognitive impairment in PD. DATA EXTRACTION: Studies were reviewed for study design, number of subjects, outcome measures, dosage, side-effects, particularly, worsening of PD motor symptoms. CONCLUSION: The strongest evidence for the pharmacological treatment of cognitive impairment and dementia in PD supports the use of cholinesterase inhibitors. Evidence for the efficacy and safety of other agents in PD dementia is either insufficient or inconclusive, but offers intriguing clues for potential future treatments. No reports from the Cochrane Collaboration were found.
ESTHER : Leroi_2006_J.Neurol.Sci_248_104
PubMedSearch : Leroi_2006_J.Neurol.Sci_248_104
PubMedID: 16806271

Title : CAMs and FGF cause a local submembrane calcium signal promoting axon outgrowth without a rise in bulk calcium concentration - Archer_1999_Eur.J.Neurosci_11_3565
Author(s) : Archer FR , Doherty P , Collins D , Bolsover SR
Ref : European Journal of Neuroscience , 11 :3565 , 1999
Abstract : Binding of basic fibroblast growth factor (bFGF) and cell adhesion molecules to the nerve cell membrane promotes axon outgrowth. This response can be blocked by antagonists of voltage-gated calcium channels, yet no change of cytosolic calcium concentration in the growth cone can be detected upon binding of the growth factor bFGF or the cell adhesion molecule L1. Using barium as a charge carrier, we show that bFGF and L1 open a calcium influx pathway in growth cones of rat sensory neurons without changing the membrane voltage. L1 does not activate influx in cells expressing a dominant negative mutant of the fibroblast growth factor receptor (FGFR) tyrosine kinase. FGFR-activated influx is blocked by specific antagonists of L- and N-type voltage-gated calcium channels and by an inhibitor of diacylglycerol lipase. We propose that both L1 and bFGF act via the FGFR to generate polyunsaturated fatty acids which in turn cause calcium channels to flicker open and shut. Short-lived domains of raised calcium at the cytosolic mouth of open channels activate axon outgrowth without raising bulk cytosolic calcium concentration. In confirmation of this model, the rapidly-acting calcium buffer BAPTA is significantly more effective at blocking FGF-induced axon outgrowth when compared with the slower buffer EGTA. Generation of short-lived calcium domains may provide a crucial mechanism for axon guidance during development and for promoting regeneration of damaged axons.
ESTHER : Archer_1999_Eur.J.Neurosci_11_3565
PubMedSearch : Archer_1999_Eur.J.Neurosci_11_3565
PubMedID: 10564364

Title : Deficiency of lecithin:cholesterol acyltransferase due to compound heterozygosity of two novel mutations (Gly33Arg and 30 bp ins) in the LCAT gene -
Author(s) : Wiebusch H , Cullen P , Owen JS , Collins D , Sharp PS , Funke H , Assmann G
Ref : Hum Mol Genet , 4 :143 , 1995
PubMedID: 7711728
Gene_locus related to this paper: human-LCAT

Title : Regional binding of 4-diphenylacetoxy-N-methylpiperidine methobromide (4-DAMP) to muscarinic receptors in rat brain and comparative analysis of minimum energy conformations - Collins_1993_Neurochem.Int_22_237
Author(s) : Collins D , Smith DA , Messer WS, Jr.
Ref : Neurochem Int , 22 :237 , 1993
Abstract : The binding of the muscarinic antagonist 4-diphenylacetoxy-N-methylpiperidine methobromide (4-DAMP), which has been suggested as an M3-selective antagonist in peripheral tissues, was examined through quantitative autoradiographic techniques in brain. The ability of 4-DAMP to displace [3H](R)-quinuclindinyl benzilate (QNB) binding to rat brain sections was compared with the known distribution of M1 and M2 muscarinic receptor subtypes as measured previously with pirenzepine and AF-DX 116 (Messer et al., 1989a). 4-DAMP displayed a high affinity for [3H](R)-QNB binding sites in rat brain sections. Analysis of 4-DAMP binding to various brain regions revealed heterogeneous binding profiles, suggesting an interaction with multiple receptor sites. Quantification of the autoradiograms indicated that 4-DAMP bound with the highest affinity to muscarinic receptors in the midline thalamus (IC50 values < 30 nM), and had a slightly lower affinity for hippocampal receptors (IC50 values between 30 and 46 nM). 4-DAMP also displayed a lower affinity for cortical receptors with IC50 values between 30 and 50 nM. The binding profile of the putative M3 muscarinic antagonist did not exhibit a marked selectivity for any single region of brain. The data suggest that whereas 4-DAMP may be selective for M3 receptors in peripheral tissues, it has limited selectivity in the CNS. Minimum energy conformations for 4-DAMP were calculated using molecular mechanics calculations. 4-DAMP displayed two global minimum energy conformations, differing in the relative position of the piperidine ring with respect to the aromatic rings. The minimum energy conformations of 4-DAMP were compared with conformations generated for pirenzepine (Messer et al., 1989a). The lowest energy conformation of 4-DAMP was superimposable on the lowest energy conformation of pirenzepine (RMS = 0.297 A). It is suggested that the conformations available to 4-DAMP permit binding to several muscarinic receptors in the CNS.
ESTHER : Collins_1993_Neurochem.Int_22_237
PubMedSearch : Collins_1993_Neurochem.Int_22_237
PubMedID: 8443567