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NOTEWORTHY ARTICLES 2004

Neurobiology of Lipids 'Noteworthy' section alerts interested readers about the selected noteworthy original research (not review) articles and meeting reports (published in other journals) on the subject of the Neurobiology of Lipids scope.

The reference to each article may be accompanied by the referee name (a member of the Neurobiology of Lipids editorial board or a journal reader), the authors' key note comments, the date of the 'noteworthy' alert, and NoL letter to editor, and links to related articles (if any).

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Noteworthy pages readership 1 January 2003 - 1 February 2005: 4742


26 December 2004

Cholesterol Sensitivity and Lipid Raft Targeting of Kir2.1 Channels
Victor G. Romanenko, Yun Fang, Fitzroy Byfield, Alexander J. Travis, Carol A. Vandenberg, George H. Rothblat, and Irena Levitan
Biophysical Journal (2004) 87(6): 3850-3861 doi:10.1529/biophysj.104.043273
[PubMed] [Abstract/FullText] [Authors contact]
 
Abstract:

"This study investigates how changes in the level of cellular cholesterol affect inwardly rectifying K+ channels belonging to a family of strong rectifiers (Kir2). In an earlier study we showed that an increase in cellular cholesterol suppresses endogenous K+ current in vascular endothelial cells, presumably due to effects on underlying Kir2.1 channels. Here we show that, indeed, cholesterol increase strongly suppressed whole-cell Kir2.1 current when the channels were expressed in a null cell line. However, cholesterol level had no effect on the unitary conductance and only little effect on the open probability of the channels. Moreover, no cholesterol effect was observed either on the total level of Kir2.1 protein or on its surface expression. We suggest, therefore, that cholesterol modulates not the total number of Kir2.1 channels in the plasma membrane but rather the transition of the channels between active and silent states. Comparing the effects of cholesterol on members of the Kir2.x family shows that Kir2.1 and Kir2.2 have similar high sensitivity to cholesterol, Kir2.3 is much less sensitive, and Kir2.4 has an intermediate sensitivity. Finally, we show that Kir2.x channels partition virtually exclusively into Triton-insoluble membrane fractions indicating that the channels are targeted into cholesterol-rich lipid rafts."

selected by Alexei Koudinov | Global Newsstand Record


26 December 2004

The LXR ligand T0901317 decreases amyloid beta production in vitro and in a mouse model of Alzheimer's disease
Radosveta P. Koldamova, Iliya M. Lefterov, Matthias Staufenbiel, Daren Wolfe, Shaohua Huang, Joseph C. Glorioso, Michael Walter, Michael G. Roth, and John S. Lazo
J Biol Chem (22 Nov 2004) doi: 10.1074/jbc.M411420200
[PubMed] [Abstract/FullText] [Authors contact]
 
Abstract:

"Recent studies indicate that oxysterols, which are ligands for the nuclear hormone liver X receptors (LXR), decrease Abeta secretion in vitro. The effect was attributed primarily to the ABCA1 transporter, transcriptionally upregulated by ligand activated LXRs. We now examined the effect of the synthetic LXR ligand T0901317, which can be used in vivo, on Abeta production in vitro and in APP23 transgenic mice. T0901317 applied to a variety of in vitro models, including immortalized fibroblasts from Tangier patients and primary embryonic mouse neurons caused a concentration-dependent decrease in Abeta secretion and this effect was increased by the addition of apolipoprotein A-I. The inhibition of Abeta production by T0901317 was cell type specific being more prominent in primary neurons than in non-neuronal cells. Tangier fibroblasts lacking a functional ABCA1 secreted more Abeta than control fibroblasts, thus demonstrating the role of ABCA1 in APP processing and Abeta generation. T0901317 treatment of 11 week old APP23 mice for 6 days showed a significant increase in ABCA1 expression and a decrease in the ratio of sAPPbeta- to sAPPalpha- cleavage products. Most importantly, the treatment caused statistically significant reduction in the levels of soluble Abeta40 and Abeta42 in the brain of these mice. Our experiments demonstrate that T0901317 decreases amyloidogenic processing of APP in vitro and in vivo, thus supporting the search for potent and specific LXR ligands with properties allowing therapeutic application."

selected by Alexei Koudinov | Global Newsstand Record


26 December 2004

Impaired Recycling of Apolipoprotein E4 Is Associated with Intracellular Cholesterol Accumulation
Joerg Heeren, Thomas Grewal, Alexander Laatsch, Nils Becker, Franz Rinninger, Kerry-Anne Rye, Ulrike Beisiegel
J Biol Chem (12 Oct 2004 / 31 Dec 2004) 279(53): 55483-92 doi:10.1074/jbc.M409324200
[PubMed] [Abstract/FullText] [Authors contact]
 
Abstract:

"After internalization of triglyceride-rich lipoproteins (TRL) in hepatoma cells, TRL particles are immediately disintegrated in the early endosomal compartment. This involves the targeting of lipids and apoprotein B along the degradative pathway and the recycling of TRL-derived apoE through recycling endosomes. Re-secretion of apoE is accompanied by the concomitant association of apoE and cellular cholesterol with high-density lipoproteins (HDL). Since epidemiological data showed that apoE3 and apoE4 have differential effects on HDL metabolism, we investigated whether the intracellular processing of TRL-derived apoE4 differs from apoE3-TRL. In this study, we demonstrated by radioactive and immunofluorescence uptake experiments that cell-surface binding and internalization of TRL-derived apoE4 are increased compared with apoE3 in hepatoma cells. Pulse-chase experiments revealed that HDL-induced recycling, but not disintegration and degradation, of apoE4-enriched TRL is strongly reduced in these cells. Furthermore, impaired HDL-induced apoE4 recycling is associated with reduced cholesterol efflux. Studies performed in Tangier fibroblasts showed that apoE recycling does not depend on ATP-binding cassette transporter A1 activity. These studies provide initial evidence that impaired recycling of apoE4 could interfere with intracellular cholesterol transport and contribute to the pathophysiological lipoprotein profile observed in apoE4 homozygotes."

selected by Alexei Koudinov | Global Newsstand Record


26 December 2004

Functional overexpression of gamma-secretase reveals protease independent trafficking functions and a critical role of lipids for protease activity
Jonathan D.J. Wrigley, Irina Schurov, Emma J. Nunn, Agnes C. L. Martin, Earl E. Clarke, Semantha Ellis, Timothy P. Bonnert, Mark S. Shearman, and Dirk Beher
J Biol Chem (21 Dec 2004) doi: 10.1074/jbc.M413086200
[PubMed] [Abstract/FullText] [Authors contact]
 
Abstract:

"Presenilins appear to form the active center of g-secretase but require the presence of the integral membrane proteins nicastrin, anterior pharynx defective 1 and presenilin enhancer 2 for catalytic function. We have simultaneously overexpressed all of these polypeptides and demonstrate functional assembly of the enzyme complex, a substantial increase in enzyme activity and binding of all components to a transition state analogue g-secretase inhibitor. Co-localization of all components can be observed in the Golgi compartment and further trafficking of the individual constituents seems to be dependent on functional assembly. Apart from its catalytic function g-secretase appears to play a role in the trafficking of the gamma-amyloid precursor protein which was changed upon reconstitution of the enzyme, but unaffected by pharmacological inhibition. Since the relative molecular mass and stoichiometry of the active enzyme complex remain elusive we performed size exclusion chromatography of solubilised g-secretase which yielded evidence of a tetrameric form of the complex, yet almost completely abolished enzyme activity. g-Secretase activity was reconstituted upon addition of an independent size exclusion chromatography fraction of lower relative molecular weight and non-proteinaceous nature, which could be replaced by a brain lipid extract. The same treatment was able to restore enzyme activity after immunoaffinity purification of the g-secretase complex demonstrating that lipids play a key role in preserving the catalytic activity of this protease. Furthermore, these data show that it is important to discriminate between intact, inactive g-secretase complexes and the active form of the enzyme, indicating the care that must be taken in the study of g-secretase."

selected by Alexei Koudinov | Global Newsstand Record


7 December 2004

Apolipoprotein A beta: Black sheep in a good family
Anatol Kontush
Brain Pathology (Oct 2004) 14(4): 433-447
[PubMed] [Abstract/FullText] [Related articles: 1 | 2 | 3 ] [Author contact]
 
Abstract:

"Amyloid-beta (Abeta, Ab) has for a long time been thought to play a central role in the pathogenesis of Alzheimer disease (AD). Analysis of available data indicates that Abeta possesses properties of a metal-binding apolipoprotein influencing lipid transport and metabolism. Protection of lipoproteins from oxidation by transition metals, synaptic activity and role in the acute phase response represent plausible physiological functions of Abeta. However, these important biochemical qualities which may critically influence the development of AD, have been largely ignored by mainstream AD researchers, making Abeta appear to be a "black sheep" in a "good apolipoprotein" family. New studies are needed to shed further light on the physiological role of Abeta in lipid metabolism in the brain."

selected by Alexei Koudinov | Global Newsstand Record


26 December 2004

Cholesterol Modulates Human Intestinal Sodium-Dependent Bile Acid Transporter
Waddah A. Alrefai, Zaheer Sarwar, Sangeeta Tyagi, Seema Saksena, Pradeep K. Dudeja, and Ravinder K. Gill
AJP: GI (16 Dec 2004) doi: 10.1152/ajpgi.00379.2004
[PubMed] [Abstract/FullText] [Authors contact]
 
Abstract:

"Bile acids are efficiently absorbed from the intestinal lumen via the ileal Apical Sodium-Dependent Bile Acid Transporter (ASBT). ASBT function is essential for maintenance of cholesterol homeostasis in the body. The molecular mechanisms of the direct effect of cholesterol on human ASBT function and expression are not entirely understood. The present studies were undertaken to establish a suitable in vitro experimental model to study human ASBT function and its regulation by cholesterol. Luminal membrane bile acid transport was evaluated by the measurement of sodiumdependent 3H-taurocholic (TC) uptake in human intestinal Caco2 cell monolayers. The relative abundance of hASBT mRNA was determined by real time PCR. Transient transfection and luciferase assay techniques were employed to assess hASBT promoter activity. Caco2 cell line was found to represent a suitable model to study hASBT function and regulation. 25-hydroxycholesterol (25-HCH, 2.5 mg/ml for 24h) significantly inhibited Na+-dependent 3H-TC uptake in Caco2 cells. This inhibition was associated with a 50 % decrease in the Vmax of the transporter with no significant changes in the apparent Km. The inhibition in hASBT activity was associated with reduction in both the level of hASBT mRNA and its promoter activity. Our data show the inhibition of hASBT function and expression by 25-hydroxycholesterol in Caco2 cells. These data provide novel evidence for the direct regulation of human ASBT function by cholesterol and suggest that this phenomenon may play a central role in cholesterol homeostasis."

selected by Alexei Koudinov | Global Newsstand Record


7 December 2004

Neuronal membrane cholesterol loss enhances amyloid peptide generation
Jose Abad-Rodriguez, Maria Dolores Ledesma, Katleen Craessaerts, Simona Perga, Miguel Medina, Andre Delacourte, Colin Dingwall, Bart De Strooper, and Carlos G. Dotti
J Cell Biol 6 December 2004 167(5): 953-960
[PubMed] [Abstract/FullText] [Related articles: 1 | 2 | 3 ] [Authors contact]
 
Keynote by Jose Abad-Rodriguez and Maria-Dolores Ledesma:

"We here provide evidence that cholesterol-rich membrane domains (rafts) act as "basins" to segregate the APP-b-secretase BACE from its substrate APP. A mild but significant reduction of membrane cholesterol observed in Alzheimer's disease patient brains or induced in cultured neurons, leads to raft disorganization. Such an alteration results in increased amyloid production. These data suggest that approaches aimed to prevent neuronal cholesterol loss, contrarily to what has been proposed, should be taken into account when considering AD treatments."

selected by Alexei Koudinov | Global Newsstand Record


31 October 2004

Serum lipids and hippocampal volume: The link to Alzheimer's disease?
Wolf H, Hensel A, Arendt T, Kivipelto M, Winblad B, Gertz HJ.
Ann Neurol. 25 Oct 2004 56(5): 745-749. doi: 10.1002/ana.20289
[PubMed] [Abstract/FullText] [Related articles: 1 | 2 | 3A, 3B] [Authors contact]
 
Keynote by Henrike Wolf:

"Disturbances in brain cholesterol metabolism have been associated with all principal pathological features of Alzheimer's disease (AD). Although serum and brain cholesterol are classically believed to be independent, some studies suggested a link between serum cholesterol and AD-like pathology or risk of dementia. In light of these findings, we studied the association between hippocampal volume - as a presumed index of AD pathologyv - and serum cholesterol in 86 elderly subjects with a range of cognitive functions. Serum HDL-cholesterol, but not LDL- or total cholesterol, was associated with hippocampal volume and dementia. This is compatible with protective effects of HDL-cholesterol on hippocampal atrophy and Alzheimer's disease. The finding could reflect the role of cholesterol and lipoproteins in facilitating synaptic plasticity in the aging human brain."

selected by Alexei Koudinov | Global Newsstand Record


29 September 2004

Do Open-Access Articles Have a Greater Research Impact?
Park P, Penick EC, Edwards JG, Kauer JA, Ehlers MD
College and Research Libraries Sept 2004 65(5) Journal FileID=31968
[Abstract] [Free FullText (.PDF)] [Related article 1 | OA News | NoL section on OA] [Author contact]
 
Abstract key note:

"Although many authors believe that their work has a greater research impact if it is freely available, studies to demonstrate that impact are few. This study looks at articles in four disciplines at varying stages of adoption of open access --philosophy, political science, electrical and electronic engineering and mathematics-- to see whether they have a greater impact as measured by citations in the ISI Web of Science database when their authors make them freely available on the Internet. The finding is that, across all four disciplines, freely available articles do have a greater research impact. Shedding light on this category of open access reveals that scholars in diverse disciplines are adopting open-access practices and being rewarded for it."

selected by Alexei Koudinov


24 September 2004

Recycling Endosomes Supply AMPA Receptors for LTP
Park P, Penick EC, Edwards JG, Kauer JA, Ehlers MD
Science 24 Sept 2004 305(5692): 1972-1975. doi: 10.1126/science.1102026
[PubMed] [Summary/FullText] [Related articles: 1 | 2 | 3 ] [Authors contact]
 
"Membrane Recycling - Memory's Key?" (keynote by Mike Ehlers):

"During long-term potentiation (LTP), the neurophysiological correlate of memory, synaptic efficacy is enhanced by the physical insertion of AMPA receptors at the postsynaptic membrane. In their recent paper in Science,  Park et al. show that recycling endosomes are the source of AMPA receptors for LTP. Transport through recycling endosomes maintains AMPA receptors at excitatory synapses and is required to "awaken" silent synapses. Blocking transport out of recycling endosomes traps AMPA receptors in neuronal dendrites, prevents stimulus-dependent AMPA receptor insertion, and completely abolishes LTP at CA1 hippocampal synapses. Moreover, stimuli that trigger LTP accelerate the recycling of AMPA receptors and also general endocytic recycling in hippocampal neurons. By coupling synaptic potentiation with membrane remodeling, LTP-induced transport from recycling endosomes to the plasma membrane provides an appealing unifying mechanism for activity-dependent synapse modification."

selected by Alexei Koudinov


30 August 2004

Association of g-secretase with lipid rafts in post-Golgi and endosome membranes
Vetrivel KS, Cheng H, Lin W, Sakurai T, Li T, Nukina N, Wong PC, Xu H, Thinakaran G.
J Biol Chem. 17 August 2004. doi: 10.1074/jbc.M407986200
[PubMed] [Abstract/FullText] [Authors contact]

selected by Alexei Koudinov


30 August 2004

Internalization of Exogenously Added Memapsin 2 ({beta}-Secretase) Ectodomain by Cells Is Mediated by Amyloid Precursor Protein
Huang X-P, Chang W-P, Koelsch G, Turner RT, III, Lupu F, Tang J.
J Biol Chem. 3 Sept 2004 279(36): 37886-37894.
[PubMed] [Abstract/FullText] [Authors contact]

selected by Alexei Koudinov


16 August 2004

Loss of Apolipoprotein E Receptor LR11 in Alzheimer Disease
Scherzer CR, Offe K, Gearing M, Rees HD, Fang G, Heilman CJ, Schaller C, Bujo H, Levey AI, Lah JJ.
Arch Neurol August 2004 61(8): 1200-1205.
[PubMed] [Abstract/FullText] [Commentary] [Related NoLs: 1 | 2 ] [Authors contact]

selected by Alexei Koudinov


8 August 2004

Physiological roles of amyloid-beta and implications for its removal in Alzheimer's disease
Bishop GM, Robinson SR.
Drugs Aging 2004 21(10): 621-630.
[PubMed] [Related articles: 1 | 2 | 3 ] [Authors contact]

selected by Alexei Koudinov


8 August 2004

LRP/Amyloid beta-peptide interaction mediates differential brain efflux of Abeta isoforms
Deane R, Wu Z, Sagare A, Davis J, Du Yan S, Hamm K, Xu F, Parisi M, LaRue B, Hu HW, Spijkers P, Guo H, Song X, Lenting PJ, Van Nostrand WE, Zlokovic BV.
Neuron 5 August 2004 43(3): 333-344
[PubMed] [Related articles: 1 | 2 | 3 | 4 ] [Authors contact]

selected by Alexei Koudinov


28 July 2004

Effects of dietary omega-3 polyunsaturated fatty acids on brain gene expression
Kitajka K, Sinclair AJ, Weisinger RS, Weisinger FS, Mathai M, Jayasooriya AP, Halver JE, Puskas LG.
Proc. Natl. Acad. Sci. USA 2004 101(30): 10931-10936
[PubMed] [Authors contact]

selected by Alexei Koudinov


24 July 2004

Deficiency of ABCA1 impairs apolipoprotein E metabolism in brain
Hirsch-Reinshagen V, Zhou S, Burgess BL, Bernier L, McIsaac SA, Chan JY, Tansley GH, Cohn JS, Hayden MR, Wellington CL.
J Biol Chem. 21 July 2004. doi: 10.1074/jbc.M407962200
[PubMed] [Review article by senior author] [Authors contact]
 
Keynote by Cheryl Wellington:

"ABCA1 is a cholesterol transporter that functions in the biogenesis of high-density lipoprotein (HDL) where it mediates the efflux of cholesterol and phospholipids to apolipoprotein (apo) A-I. Deficiency of ABCA1 results in lack of circulating HDL and greatly reduced levels of apoA-I. ABCA1 is also expressed in cells within the CNS, but its roles in brain lipid metabolism are not yet fully understood. In this study, we demonstrate that glial expression of ABCA1 is required for normal apoE metabolism in the brain. Deficiency of glial ABCA1 impairs cholesterol efflux to apoE, causes lipid accumulation, and inhibits apoE secretion. These defects result in an overall  reduction of apoE levels in the brain, particularly in the hippocampus and striatrum. Our results suggest that ABCA1 may affect neurodegenerative diseases by impacting apoE metablism in the CNS."

selected by Alexei Koudinov


24 July 2004

ABCA1 is required for normal CNS apoE levels and for lipidation of astrocyte-secreted apoE
Wahrle SE, Jiang H, Parsadanian M, Legleiter J, Han X, Fryer JD, Kowalewski T, Holtzman DM.
J Biol Chem. 21 July 2004. doi: 10.1074/jbc.M407963200
[PubMed] [Authors contact]

selected by Alexei Koudinov


27 June 2004

Lipids make smooth brains gyrate
Price DJ.
Trends Neurosci July 2004 27(7): 362-364
[PubMed] [Author contact]

selected by Ilya Reznik


15 June 2004

Carpe Diem. Retooling the "Publish or Perish" Model into the "Share and Survive" Model
Rhee SY.
Plant Physiology February 2004 134: 543-547
[PubMed] [FullText] [Author contact]

selected by Alexei Koudinov


14 June 2004

Involvement of Notch signaling in hippocampal synaptic plasticity
Wang Y, Chan SL, Miele L, Yao PJ, Mackes J, Ingram DK, Mattson MP, Furukawa K.
Proc Natl Acad Sci USA. 9 June 2004. doi: 10.1073/pnas.0308126101
[PubMed] [ARF comment] [Authors: contact | web site 1 | 2]
 
Keynote by Katsutoshi Furukawa:

"Notch is a transmembrane receptor involved in cell fate decisions during development including neurogenesis and neuronal develpment.  Although Notch signaling has been proposed to play a critical role in the developing nervous system, the function of Notch in the mature nervous system, especially regarding neuronal plasticity, has not been investigated.  We developed Notch anti-sense transgenic mice expressing lower levels of Notch protein and analyzed long term potentiation (LTP) using these mice. LTP is significantly impaired and NFkB levels are lower in the mice with reduced Notch than in control mice. These results suggest that Notch signaling directly regulates synaptic plasticity, which is considered to be associated with learning and memory in the mature nervous system."

selected by Alexei Koudinov


13 June 2004

Transgenic mice overexpressing amyloid beta protein are an incomplete model of Alzheimer disease
Schwab C, Hosokawa M, McGeer PL.
Exp Neurol July 2004 188(1): 52-64
[PubMed] [SummaryPlus] [FullText] [Related articles: 1 | 2 | 3 | 4 | 5 ] [Authors contact]
 
Keynote by Patrick L. McGeer:

"In this study a direct comparison was made between the pathology of Alzheimer's disease (AD) and that of two transgenic mouse models (APP23 and tg2576) that develop extracellular beta amyloid deposits. While a great similarity was found in immunostaining for beta-amyloid, very significant differences were noted using other markers of pathology. The greatest contrasts were found in a failure of the mouse models to show any evidence of neurofibrillary tangles or any obvious sign of neuronal loss. The models do not bear out predictions of the amyloid hypothesis of AD, which holds that beta amyloid is toxic and is responsible for inducing the neurofibrillary tangles of AD. But they are consistent with independent studies of early AD in which it has been clearly established that tangles precede plaques. The differences in pathology between the mouse models and actual AD suggest that therapeutic approaches to AD that exclusively target beta amyloid may be naive."

selected by Alexei Koudinov  | Related NoL Subject collection


16 May 2004

Cholesterol metabolism in the central nervous system during early development and in the mature animal
Dietschy JM, Turley SD.
J Lipid Res. 17 May 2004. doi: 10.1194/jlr.R400004-JLR200
[PubMed] [Authors contact]

selected by Alexei Koudinov


14 May 2004

Differential expression of cholesterol hydroxylases in Alzheimer's disease
Brown J, Theisler C, Silberman S, Magnuson D, Gottardi-Littell N, Lee JM, Yager D, Crowley J, Sambamurti K, Rahman MM, Reiss AB, Eckman CB, Wolozin B.
J Biol Chem. 17 May 2004. doi: 10.1074/jbc.M402324200
[PubMed] [Authors contact]

selected by Alexei Koudinov


20 February 2004

Niemann-Pick C1 Like 1 Protein Is Critical for Intestinal Cholesterol Absorption
Altmann SW, Davis HR Jr., Zhu L-J, Yao X, Hoos LM, Tetzloff G, Iyer SPN, Maguire M, Golovko A, Zeng M, Wang L, Murgolo N, and Graziano MP.
Science 20 Feb 2004 303: 1201-1204. doi: 10.1126/science.1093131
[PubMed] [FullText] [Commentary: 1] [Authors contact]
 
Keynote by "This week in Science":

"The statins, a class of widely prescribed drugs that inhibit cholesterol biosynthesis, have proved very effective in reducing serum levels of cholesterol. However, because statins are not safe for all patients, and because not all patients respond to these drugs, alternative cholesterol-lowering strategies are being sought. In a study exploring the mechanism by which dietary cholesterol is absorbed from the intestine, Altmann et al. (p. 1201; see the Perspective by Klett and Patel) identified a protein, NPC1L1 (Niemann-Pick C1 Like 1), with sequence and expression features expected of an intestinal cholesterol transporter. Mice genetically deficient in NPC1L1 exhibited a 70% reduction in absorbed cholesterol and were insensitive to ezetimibe, a drug that blocks cholesterol absorption but whose molecular target is unknown. Further analysis of NPC1L1 and other proteins in its cellular pathway may lead to more effective drugs for cholesterol management."

selected by Alexei Koudinov


20 February 2004

Involvement of oxidative stress-induced abnormalities in ceramide and cholesterol metabolism in brain aging and Alzheimer's disease
Cutler RG, Kelly J, Storie K, Pedersen WA, Tammara A, Hatanpaa K, Troncoso JC, and Mattson MP.
Proc Natl Acad Sci USA. 17 Feb 2004 101: 2070-2075.
[PubMed] [ARF comments] [Authors contact]

Also see related Neuroscience 2002, 2003 meeting abstracts by the authors: 1 | 2

selected by Alexei Koudinov


16 February 2004

Formation of 7-dehydrocholesterol-containing membrane rafts in vitro and in vivo, with relevance to the Smith-Lemli-Opitz syndrome
Keller R, Arnold TP, and Fliesler SJ.
J Lip Res 2004 45: 347-355
[PubMed] [Abstract/FullText] [Authors contact]

selected by Alexei Koudinov


12 February 2004

Brain metabolic decreases related to the dose of the ApoE e4 allele in Alzheimer’s disease
Mosconi BL, Nacmias B, Sorbi S, De Cristofaro MTR, Fayazz M, Tedde A, Bracco L, Herholz K, and Pupi A.
J Neurol Neurosurg Psych (JNNP) Jan 2004 75: 370-376
[PubMed] [Abstract/FullText] [Authors contact]

selected by Ilya Reznik


6 February 2004

Changes in apolipoprotein E expression in response to dietary and pharmacological modulation of cholesterol
Petanceska S, DeRosa S, Sharma A, Diaz N, Duff K, Tint SG, Refolo LM, Pappolla M.
J Mol Neurosci 2003 20: 395-406.
[PubMed] [Authors contact]

selected by Alexei Koudinov


4 February 2004

Squalestatin cures prion-infected neurones and protects against prion neurotoxicity
Bate C, Salmona M, Diomede L, and Williams A.
J Biol Chem 29 Jan 2004 279(15): 14983-90. Doi: 10.1074/jbc.M313061200
[PubMed] [FullText] [Related articles: 1] [Authors contact]

selected by Luisa Diomede


25 January 2004

Reduced Hippocampal Insulin-Degrading Enzyme in Late-Onset Alzheimer’s Disease Is Associated with the Apolipoprotein E-e4 Allele.
Cook DG, Leverenz JB, McMillan PJ, Kulstad JJ, Ericksen S, Roth RA, Schellenberg GD, Jin L-W, Kovacina KS and Craft S.
Am J Pathol Jan 2003 162: 313-319.
[PubMed] [FullText] [Related article: 1 | 2 | 3] [ARF content: 1 | 2 | 3] [Authors contact]

selected by Alexei Koudinov


25 January 2004

b-Amyloid prevents excitotoxicity via recruitment of glial glutamate transporters.
Baba A, Mitsumori K, Yamada MK, Nishiyama N, Matsuki N and Ikegaya Y.
Archives of Pharmacology 4 Sept 2003 368(3): 234-238. doi: 10.1007/s00210-003-0792-6
[PubMed] [Abstract] [FullText] [Related articles: 1 | 2 | 3 | 4 | 5] [Authors contact]
 
Keynote by Atsushi Baba:

"Amyloid beta-protein (A-beta), a peptide with 42 residues that appears to be pathogenic in AD dementia, is recently shown to induce a substantial increase in the glutamate uptake activity of astrocytes by translocating GLAST, a type of glial glutamate transporters, to the plasma membrane.  We found that pre-treatment of neuro-astroglial co-cultures with low, but pathophysiologically relevant, concentrations of A-beta protects neurons against excitotoxic insults by enhancing the clearance rate of extracellular glutamate. The data provide evidence that the ability of glia to uptake glutamate is directly related with excitotoxicity and also are consistent with a recent concept that A-beta-induced neuron loss cannot account for the early phase in AD dementia."

selected by Alexei Koudinov


25 January 2004

A liver X receptor and retinoid X receptor heterodimer mediates apolipoprotein E expression, secretion and cholesterol homeostasis in astrocytes.
Liang Y, Lin S, Beyer TP, Zhang Y, Wu X, Bales KR, DeMattos RB, May PC, Li SD, Jiang XC, Eacho PI, Cao G, Paul SM.
J Neurochem Feb 2004 88(3): 623-624.
[PubMed] [Authors contact]

selected by Alexei Koudinov


25 January 2004

Cognitive impairment associated with atorvastatin and simvastatin.
King DS, Wilburn AJ, Wofford MR, Harrell TK, Lindley BJ, Jones DW.
Pharmacotherapy Dec 2003 23(12): 1663-1667.
[PubMed][Authors contact]

selected by Alexei Koudinov


23 January 2004

Rod photoreceptor responses in children with Smith-Lemli-Opitz syndrome.
Elias ER, Hansen RM, Irons M, Quinn NB, Fulton AB.
Arch Ophthalmol Dec 2003 121(12): 1738-1743.
[PubMed] [Authors contact]

selected by Temirbolat Berezov


23 January 2004

Glial lipoproteins stimulate axon growth of central nervous system neurons in compartmented cultures
Hayashi H, Campenot RB, Vance DE, and Vance JE.
J Biol Chem ePub 6 Jan 2004 doi: 10.1074/jbc.M313828200; 2 Apr 2004 279: 14009-15.
[PubMed][FullText] [Related article: 1][Authors contact]
 
Keynote by Jean Vance:

"The role played by lipoproteins secreted by cortical glial cells in axon growth of central nervous system neurons was investigated.  When apo E-containing lipoproteins secreted by glial cells were added to distal axons, but not cell bodies, of retinal ganglion cells cultured in compartmented dishes, axon extension was increased by 50%.  Inhibition of cholesterol synthesis in glial cells diminished the secretion of apo E and cholesterol and prevented the growth stimulatory effect of glial cell-conditioned medium.  The stimulation of axon growth was abrogated in the presence of receptor-associated protein (RAP) indicating an involvement of receptor(s) of the low density lipoprotein receptor family in stimulation of axonal extension."

selected by Temirbolat Berezov


23 January 2004

The levels of soluble Ab in different HDL subfractions distinguish Alzheimer's and normal aging CSF: implication for brain cholesterol pathology?
Koudinov AR, Berezov TT, Koudinova NV.
Neurosci Lett 2001 314: 115-118.
[PubMed] [FullText] [ Related NoL: 1 ] [Authors contact]

selected by Temirbolat Berezov


22 January 2004

ApoE and clusterin cooperatively suppress Abeta levels and deposition: evidence that ApoE regulates extracellular Abeta metabolism in vivo.
DeMattos RB, Cirrito JR, Parsadanian M, May PC, O'Dell MA, Taylor JW, Harmony JAK, Aronow BJ, Bales KR, Paul SM, Holtzman D.
Neuron 22 Jan 2004 41: 193-202.
[PubMed] [FullText] [Related article: 1 | 2 | 3 | 4 | 5] [ARF content: 1 | 2 | 3 | 4 | 5 | 6] [Authors: patent | contact]

selected by Alexei Koudinov


21 January 2004

Soluble Ab homeostasis in AD and DS: impairment of anti-amyloidogenic protection by lipoproteins.
Matsubara E, Sekijima Y, Tokuda T, Urakami K, Amari M, Shizuka-Ikeda M, Tomidokoro Y, Ikeda M, Kawarabayashi T, Harigaya Y, Ikeda S, Murakami T, Abe K, Otomo E, Hirai S, Frangione B, Ghiso J.
Neurobiol Aging ePub 16 Jan 2004 doi:10.1016/j.neurobiolaging.2003.10.004.
[PubMed] [FullText] [Related articles: 1 | 2 | 3 | 4 | 5] [Authors contact]

selected by Anatol Kontush


12 January 2004

Residential Environments and Cardiovascular Risk.
Ana V. Diez Roux
J Urban Health 2003 80(4): 569-589.
[Abstract] [Authors contact]

selected by Temirbolat Berezov


12 January 2004

Incorporation of docosahexaenoic acid into nerve membrane phospholipids: bridging the gap between animals and cultured cells.
Alessandri J-M, Poumès-Ballihaut C, Langelier B, Perruchot M-H, Raguénez G, Lavialle M, and Guesnet P.
Am J Clinical Nutrition Oct 2003 78: 702-710.
[PubMed] [ FullText ] [ Related articles: 1 | 2 ] [Authors contact]

selected by Temirbolat Berezov



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