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AGPS  -  alkylglycerone phosphate synthase

Homo sapiens

Synonyms: AAG5, ADAP-S, ADAS, ADHAPS, ADPS, ...
 
 
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Disease relevance of AGPS

 

Psychiatry related information on AGPS

  • Primary endpoints were cognition (Alzheimer's disease assessment scale, cognitive subscale [ADAS-cog]) and global functioning (clinician's interview-based impression of change plus caregiver input [CIBIC-plus]) [4].
  • Efficacy, assessed by the Alzheimer's Disease Assessment Scale-cognitive subscale (ADAS-cog) and Clinical Dementia Rating-Sum of the Boxes (CDR-SB), was examined in comparison with published data of untreated AD patients [5].
  • Other psychometric tests (trailmaking test, ADAS, CGI) and electrophysiological investigations (EEG topography) were evaluated descriptively [6].
  • Secondary outcome measures were the ADAS cognitive (ADAS-Cog) and noncognitive score (ADAS-Noncog), the clinical global response (CGI-Improvement), the SKT neuropsychological test battery, and the Nurses' Observation Scale for Geriatric Patients (NOSGER-Total and IADL subscale) [7].
  • RESULTS: Patients with probable vascular dementia treated with galantamine for 6 or 12 months showed significant improvements in ADAS-cog/11 scores versus baseline, which were maintained at the end of the 12-month study [8].
 

High impact information on AGPS

  • Among patients receiving 80 mg/d of tacrine, 51% achieved a four-point or greater improvement of the ADAS cognitive component after 12 weeks of treatment [9].
  • In addition, low levels of palmitoyl-DHAP (less than 100 microM) show competitive inhibition with respect to hexadecanol, possibly due to palmitic acid formed from palmitoyl-DHAP by alkyl-DHAP synthase under these conditions [10].
  • The use of donepezil produced statistically significant improvements in ADAS-cog, CIBIC plus, and Mini-Mental State Examination scores, relative to placebo [11].
  • The correlations between plasma drug concentrations and both ADAS-cog (P<.001) and CIBIC plus (P = .006) were also statistically significant, as were the correlations between red blood cell acetylcholinesterase inhibition and change in ADAS-cog (P<.001) and CIBIC plus (P = .005) [11].
  • Diurnal changes in sucrose, nucleotides, starch synthesis and AGPS transcript in growing potato tubers that are suppressed by decreased expression of sucrose phosphate synthase [12].
 

Chemical compound and disease context of AGPS

  • In the RCTs of donepezil, the mean decrease in scores on the Alzheimer's Disease Assessment Scale-cognitive subscale (ADAS-cog) was greater with active treatment than with placebo (lower scores indicate less cognitive deterioration) [13].
  • Correlations between ADAS-cog changes and P300 changes significantly separated patients treated with DPZ and Riv from those treated with vitamin E. Administration of DPZ and Riv reduced the latencies of P300 components proportionately to neuropsychologic test improvements [14].
  • However, at 26 weeks, placebo-treated APOE epsilon4 patients declined 3.04 points below baseline on the cognitive subscale of the Alzheimer's Disease Assessment Scale (ADAS-cog), and rivastigmine-treated patients improved by 1.67 points [15].
  • CONTEXT: Recent evidence suggests that treatment of mild-to-moderate Alzheimer's disease (AD) with atorvastatin provides significant benefit on the Alzheimer Disease Assessment Scale-Cognitive (ADAS-cog) after 6 months [16].
  • Active treatment in both trials was memantine at the standard daily dose of 10 mg b.i.d. The cognitive subscale of the Alzheimer's Disease Assessment Scale (ADAS-cog) was a primary endpoint in both trials, and in both trials a statistically significant difference was seen between treatment groups after 28 weeks [17].
 

Biological context of AGPS

 

Anatomical context of AGPS

 

Associations of AGPS with chemical compounds

  • Deficient de novo plasmalogen synthesis in her fibroblasts as a result of low DHAPAT activity was found, while her very-long-chain fatty acid profile, phytanic acid concentration, alkyl-dihydroxyacetonephosphate synthase (alkyl-DHAP synthase) activity, and peroxisomal 3-ketoacyl-CoA thiolase protein were normal [20].
  • RESULTS: 180 (75%) rapidly and 337 (78%) slowly progressing patients provided ADAS-cog data after 26 weeks of open-label rivastigmine treatment [21].
  • At endpoint, memantine was shown to improve cognition relative to placebo in VaD: the change of ADAS-cog from baseline differed by a mean of -1.75 points (95% confidence intervals -3.023 to -0.49) and a median of 2 points between the two groups, while CGI-C ratings showed no significant differences between treatment groups [22].
  • RESULTS: At 52 weeks, change in ADAS-cog scores from baseline was similar for placebo and celecoxib 200 mg bid groups (5.00 and 4.39, respectively) [23].
  • The association between fasting plasma homocysteine level and cognitive function was investigated by multiple linear regression analysis.RESULTS: In the crude model homocysteine concentration was not significantly related to ADAS-cog score (beta = 0.061; p = 0.45).Age was found to be related to ADAS-cog score (beta = 0.161; p < 0.05) [24].
 

Analytical, diagnostic and therapeutic context of AGPS

  • In longitudinal studies or in the course of the disease, scores assessed with the ADAS-cog and the SKT may now be statistically compared [25].
  • A significant improvement in memory performance, evaluated with items of the ADAS cog, was also found in elderly people taken a single dose of oral Cerebrolysin (6.9+/-1.0 errors at baseline versus 4.9+/-1.0 errors after treatment; p < 0.01) [26].
  • Inter-group differences in the ADAS cognitive and non-cognitive subscales did not reach statistical significance, probably because of the small sample size [6].
  • METHODS: Rapidly and slowly progressing patients were identified by rates of cognitive decline [>/=4 points and <4 points, respectively, on the Alzheimer's Disease Assessment Scale -- cognitive subscale (ADAS-cog)] during 26 weeks of placebo treatment in four randomized controlled trials (weeks 0--26) [21].
  • Certain sub-components of the ADPS are described in detail, including the aerosol collector, the automated sample preparation module that performs multiplexed immunoassays with confirmatory PCR, and the data monitoring and communications system [27].

References

  1. Immunological analyses of alkyl-dihydroxyacetone-phosphate synthase in human peroxisomal disorders. Biermann, J., Gootjes, J., Humbel, B.M., Dansen, T.B., Wanders, R.J., van den Bosch, H. Eur. J. Cell Biol. (1999) [Pubmed]
  2. Role of IVIg in autoimmune, neuroinflammatory and neurodegenerative disorders of the central nervous system: present and future prospects. Dalakas, M.C. J. Neurol. (2006) [Pubmed]
  3. The effects of a cholinesterase inhibitor are prominent in patients with fluctuating cognition: a part 3 study of the main mechanism of cholinesterase inhibitors in dementia. Onofrj, M., Thomas, A., Iacono, D., Luciano, A.L., Di Iorio, A. Clinical neuropharmacology. (2003) [Pubmed]
  4. Efficacy of galantamine in probable vascular dementia and Alzheimer's disease combined with cerebrovascular disease: a randomised trial. Erkinjuntti, T., Kurz, A., Gauthier, S., Bullock, R., Lilienfeld, S., Damaraju, C.V. Lancet (2002) [Pubmed]
  5. Long-term efficacy and safety of donepezil in the treatment of Alzheimer's disease: an interim analysis of the results of a US multicentre open label extension study. Rogers, S.L., Friedhoff, L.T. European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology. (1998) [Pubmed]
  6. Clinical efficacy of Ginkgo biloba special extract EGb 761 in dementia of the Alzheimer type. Maurer, K., Ihl, R., Dierks, T., Frölich, L. Journal of psychiatric research. (1997) [Pubmed]
  7. Sustained efficacy and safety of idebenone in the treatment of Alzheimer's disease: update on a 2-year double-blind multicentre study. Gutzmann, H., Hadler, D. J. Neural Transm. Suppl. (1998) [Pubmed]
  8. Galantamine in the treatment of cognitive decline in patients with vascular dementia or Alzheimer's disease with cerebrovascular disease. Small, G., Erkinjuntti, T., Kurz, A., Lilienfeld, S. CNS drugs. (2003) [Pubmed]
  9. A controlled trial of tacrine in Alzheimer's disease. The Tacrine Study Group. Farlow, M., Gracon, S.I., Hershey, L.A., Lewis, K.W., Sadowsky, C.H., Dolan-Ureno, J. JAMA (1992) [Pubmed]
  10. Alkyldihydroxyacetone-P synthase. Solubilization, partial purification, new assay method, and evidence for a ping-pong mechanism. Brown, A.J., Snyder, F. J. Biol. Chem. (1982) [Pubmed]
  11. Donepezil improves cognition and global function in Alzheimer disease: a 15-week, double-blind, placebo-controlled study. Donepezil Study Group. Rogers, S.L., Doody, R.S., Mohs, R.C., Friedhoff, L.T. Arch. Intern. Med. (1998) [Pubmed]
  12. Diurnal changes in sucrose, nucleotides, starch synthesis and AGPS transcript in growing potato tubers that are suppressed by decreased expression of sucrose phosphate synthase. Geigenberger, P., Stitt, M. Plant J. (2000) [Pubmed]
  13. Donepezil and rivastigmine in the treatment of Alzheimer's disease: a best-evidence synthesis of the published data on their efficacy and cost-effectiveness. Wolfson, C., Oremus, M., Shukla, V., Momoli, F., Demers, L., Perrault, A., Moride, Y. Clinical therapeutics. (2002) [Pubmed]
  14. Donepezil, rivastigmine, and vitamin E in Alzheimer disease: a combined P300 event-related potentials/neuropsychologic evaluation over 6 months. Thomas, A., Iacono, D., Bonanni, L., D'Andreamatteo, G., Onofrj, M. Clinical neuropharmacology. (2001) [Pubmed]
  15. Differential qualitative responses to rivastigmine in APOE epsilon 4 carriers and noncarriers. Farlow, M., Lane, R., Kudaravalli, S., He, Y. Pharmacogenomics J. (2004) [Pubmed]
  16. Circulating cholesterol levels, apolipoprotein E genotype and dementia severity influence the benefit of atorvastatin treatment in Alzheimer's disease: results of the Alzheimer's Disease Cholesterol-Lowering Treatment (ADCLT) trial. Sparks, D.L., Connor, D.J., Sabbagh, M.N., Petersen, R.B., Lopez, J., Browne, P. Acta Neurol. Scand., Suppl. (2006) [Pubmed]
  17. Memantine in vascular dementia. Möbius, H.J., Stöffler, A. International psychogeriatrics / IPA. (2003) [Pubmed]
  18. The dihydroxyacetonephosphate pathway for biosynthesis of ether lipids in Leishmania mexicana promastigotes. Heise, N., Opperdoes, F.R. Mol. Biochem. Parasitol. (1997) [Pubmed]
  19. Stability of alkyl-dihydroxyacetonephosphate synthase in human control and peroxisomal disorder fibroblasts. Biermann, J., Gootjes, J., Wanders, R.J., van den Bosch, H. IUBMB Life (1999) [Pubmed]
  20. Abnormal myelin formation in rhizomelic chondrodysplasia punctata type 2 (DHAPAT-deficiency). Sztriha, L., Al-Gazali, L.I., Wanders, R.J., Ofman, R., Nork, M., Lestringant, G.G. Developmental medicine and child neurology. (2000) [Pubmed]
  21. Efficacy of rivastigmine in Alzheimer's disease patients with rapid disease progression: results of a meta-analysis. Farlow, M.R., Small, G.W., Quarg, P., Krause, A. Dementia and geriatric cognitive disorders. (2005) [Pubmed]
  22. A double-blind, placebo-controlled multicentre study of memantine in mild to moderate vascular dementia (MMM500). Wilcock, G., Möbius, H.J., Stöffler, A. International clinical psychopharmacology. (2002) [Pubmed]
  23. Long-term efficacy and safety of celecoxib in Alzheimer's disease. Soininen, H., West, C., Robbins, J., Niculescu, L. Dementia and geriatric cognitive disorders (2007) [Pubmed]
  24. Homocysteine and cognitive function in institutionalised elderly A cross-sectional analysis. Manders, M., Vasse, E., de Groot, L.C., van Staveren, W.A., Bindels, J.G., Blom, H.J., Hoefnagels, W.H. European journal of nutrition. (2006) [Pubmed]
  25. Neuropsychometric tests in cross sectional and longitudinal studies - a regression analysis of ADAS - cog, SKT and MMSE. Ihl, R., Grass-Kapanke, B., Jänner, M., Weyer, G. Pharmacopsychiatry (1999) [Pubmed]
  26. Oral Cerebrolysin enhances brain alpha activity and improves cognitive performance in elderly control subjects. Alvarez, X.A., Lombardi, V.R., Corzo, L., Pérez, P., Pichel, V., Laredo, M., Hernández, A., Freixeiro, F., Sampedro, C., Lorenzo, R., Alcaraz, M., Windisch, M., Cacabelos, R. J. Neural Transm. Suppl. (2000) [Pubmed]
  27. APDS: the autonomous pathogen detection system. Hindson, B.J., Makarewicz, A.J., Setlur, U.S., Henderer, B.D., McBride, M.T., Dzenitis, J.M. Biosensors & bioelectronics. (2005) [Pubmed]
 
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