Serum lipids and hippocampal volume: The link to Alzheimer's disease?

Citation: Wolf H, Hensel A, Arendt T, Kivipelto M, Winblad B, Gertz HJ. Serum lipids and hippocampal volume: The link to Alzheimer's disease? Ann Neurol. 56(5), 745-749 (25 Oct 2004) . doi: 10.1002/ana.20289.

Abstract: The association between hippocampal volume (as a presumed index of Alzheimer's disease pathology) with serum total cholesterol, high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol was studied in 86 elderly subjects with a range of cognitive functions. High-density lipoprotein cholesterol, but not low-density lipoprotein cholesterol or total cholesterol, was associated with hippocampal volume and dementia. This is compatible with protective effects of high-density lipoprotein cholesterol on hippocampal atrophy and Alzheimer's disease.

Authors: Henrike Wolf, MD, PhD; Anke Hensel, DP; Thomas Arendt, MD, PhD; Miia Kivipelto, MD, PhD; Bengt Winblad, MD, PhD; Hermann-Josef Gertz, MD, PhD
Authors Institution: Department of Neurotec, Division of Clinical Geriatrics, Karolinska Institutet, Stockholm, Sweden, e.mail: henrike.wolf[at]neurotec.ki.se ; Department of Psychiatry, University of Leipzig, Leipzig, Germany; Paul Flechsig Institute for Brain Research, University of Leipzig, Leipzig, Germany

First author key note: "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."

Further reading: see related articles at Neurobiology of Lipids.

Scientists, consider where you publish

Citation: Seringhaus M. Scientists, consider where you publish. Neurobiol Lipids Vol. 3, 10 (2 Nov 2004). Available at: http://neurobiologyoflipids.org/content/3/10/

Abstract: For scientists, publishing a paper in a respected peer-reviewed journal marks the culmination of successful research. But some of the most prestigious and sought-after journals are so costly to access that a growing number of academic libraries can't afford to subscribe. Before submitting your next manuscript, consider a journal's access policy alongside its prestige - and weigh the implications of publishing in such costly periodicals. Two distinct problems continue to plague scientific publishing. First, institutional journal subscription costs are skyrocketing so fast that they outstrip the ability of many libraries to pay, threatening to sever scientists from the literature. Second, the taxpaying public funds a terrific amount of research in this country, and with few exceptions, can't access any of it. These problems share a common root - paid access to the scientific literature.

Author: Michael Seringhaus
Authors Institution: Department of Molecular Biophysics and Biochemistry, Yale University, 266 Whitney Avenue, New Haven CT 06520 USA. e.mail: michael.seringhaus[at]yale.edu

Key words: Free open access; STM journals archives publishing; institutional repositories; Public Library of Science PLoS; BioMed Central; PubMed Central PMC; SPARC; access price permission barrier; serials pricing crisis; US Congress; science policy; Elsevier Cell Press Immunity Neuron

Association of Research Libraries (ARL) official comments on National Institutes of Health (NIH) public access proposal

Citation: Adler PS. Association of Research Libraries (ARL) official comments on National Institutes of Health (NIH) public access proposal. Neurobiol Lipids Vol. 3, 9 (2 Nov 2004). Available at: http://neurobiologyoflipids.org/content/3/9/

Abstract: I am writing on behalf of the Association of Research Libraries (ARL) to express our strong support for the National Institutes of Health (NIH) proposal to provide freely available online access to NIH-funded manuscripts via PubMed Central, http://grants1.nih.gov/grants/guide/notice-files/NOT-OD-04-064.html. There are many aspects of the NIH plan that ARL endorses and ARL applauds NIH's leadership in promoting this balanced initiative. There are six issues concerning the NIH plan that are the focus of ARL’s comments, including how the proposal: reflects the way scientists conduct research and discovery; allows some libraries to provide additional resources to their users; creates an archival resource for biomedical literature funded by NIH; provides significant protections to commercial and not-for-profit publishers; follows congressional and administration policy; and expands and improves public access to biomedical information.

Author: Prudence S. Adler
Authors Institution: Associate Executive Director, Association of Research Libraries, 21 Dupont Circle, Suite 800, Washington, D.C. 20036, USA, e.mail: prue[at]arl.org

Key words: Free open access; STM journals archives publishing; institutional repositories; Public Library of Science PLoS; BioMed Central; PubMed Central PMC; SPARC; access price permission barrier; serials pricing crisis; US Congress; science policy; Elsevier

34th Society for Neuroscience Annual Meeting neurobiology of lipids sessions 2004

Citation: Editorial Material. 34th Society for Neuroscience Annual Meeting neurobiology of lipids sessions 2004. Neurobiol Lipids Vol. 3, 5 (13 Sep 2004). Available at: http://neurobiologyoflipids.org/content/3/5/

Abstract: This article alerts interested readers about neurobiology of lipids sessions of the 34th Society for Neuroscience (SfN) annual meeting, 23-27 October, 2004, San Diego, CA. The abstracts were retrieved from the SfN web based abstract system as a result of the search for the key words cholesterol, phospholipid, lipoprotein, apolipoprotein, fatty acid, lipid, lipid peroxidation in abstract title/key words, abstract text or session title. The reference to each abstract entry includes day/time, program number, presentation type, location, authors list, first author first affiliation, and the abstract title. Each abstract title provides link to abstract text at the scholarone.com web site. The presented list yielded editors' choice short list of noteworthy presentations. All abstracts' authors were invited to publish peer-reviewed proceedings articles in the Neurobiology of Lipids.

Author: Editorial Material
Authors Institution: Neurobiology of Lipids, P.O.Box 1665 Rehovot 76100, Israel; sfnabstracts[at]neurobiologyoflipids.org

Key words: neuroscience of lipids; literature update; cholesterol; fatty acids; fa; srebp; lxr; phospholipids; lipoprotein; lipid peroxidation; psychiatry; neurology; receptor; amyloid hypothesis; Alzheimer's disease; Down syndrome; synapse; synaptic plasticity

The use of fatty acid supplementation for seizure management

Citation: Mostofsky DI et al. The use of fatty acid supplementation for seizure management. Neurobiol Lipids Vol. 3, 4 (20 Oct 2004). Available at: http://neurobiologyoflipids.org/content/3/4/

Abstract: Impressive research demonstrates the importance of essential fatty acids (FA) for many physiological and behavioral mechanisms, in both humans and animals. In humans, essential fatty acids must be supplied via the diet. The genesis, maintenance, exacerbation, and treatment for many chronic health conditions are often related to deficiencies in omega-6 (linoleic acid) and omega-3 (alpha-linolenic acid), and their derivatives. In animal studies, providing supplementation of these FA changes chemical, immune, and structural properties of the brain, including the fluidity of the neuronal membrane. Of particular interest to epilepsy, pre-treatment of a ratio of the FA omega-3 / omega-6 resulted in altering the threshold for seizures following administration of convulsant agents that reliably induce epileptic activity. This report reviews the human and animal clinical and experimental data and theoretical considerations that support the promise for FA supplementation for use by seizure patients.

Author: David I. Mostofsky and colleagues
Authors Institution: Department of Psychology, Boston University, Boston, MA

Key words: fatty acids; FA; polyunsaturated fatty acids; ketogenic diet; omega-3; omega-6; seizures; membrane fluidity; epilepsy; anti-epileptic drug; cortisol; stress; blood-brain barrier; BBB; elongation; linoleic acid; alpha-linoleic acid; n-3; n-6

Pierre Morell tribute for neurobiology of lipids

Citation: Toews A, Jurevics H. Pierre Morell tribute for neurobiology of lipids. Neurobiol Lipids Vol. 3, 3 (19 May 2004). Available at: http://neurobiologyoflipids.org/content/3/3/

Abstract: Pierre Morell, Professor of Biochemistry and Biophysics at the University of North Carolina-Chapel Hill, passed away on July 15, 2003 after a brief illness. Pierre was educated at the Bronx High School of Science, Columbia University, and The Albert Einstein College of Medicine, doing post-doctoral research with Norm Radin at the University of Michigan-Ann Arbor. Pierre was a leader in the field of myelin metabolism, in particular the synthesis and turnover of myelin lipids (glycosphingo-lipids, phospholipids, cholesterol). A re-curring theme was use of altered states (e.g., mutant or genetically engineered mice, toxicants, altered nutritional states) to examine myelin metabolism and function. He was a tireless supporter of various scientific societies, including the International Society for Neurochemistry, and he provided wise counsel and advice to several generations of neuroscientists throughout the world. His premature passing has left a void that will be difficult to fill. A memorial fund at UNC has been established.

Author: Arrel Toews and Helga Jurevics
Authors Institution: University of North Carolina (UNC) Neuroscience Center, CB# 7250, Chapel Hill, NC 27599-7250, USA, atoews[at]med.unc.edu

Key words: memoriam; myelin; demyelination; glycosphingolipids; cerebroside; sulfatide; tellurium; Cuprizone; remyelination; cholesterol; phospholipids; lipid synthesis; lipid turnover; myelin metabolism; myelin gene expression; mutant mice; PLPnull; axonal transport

Open letter to President George W. Bush on conduct by scientists, STM journals, and Scientific Institutions

Citation: Koudinov AR. Open letter to President George W. Bush on conduct by scientists, STM journals, and Scientific Institutions. Neurobiol Lipids Vol. 3, 2 (10 March 2004). Available at: http://neurobiologyoflipids.org/content/3/2/

Abstract: Several recent publications in Science magazine seem supporting the "campaign to stop [George W. Bush Administration] misuse of science before it damages our health, safety, and environment." This open letter to The President argues that the major threat to the public health and public interest in science come from corrupted scientists, STM journals and scientific institutions. The letter quotes the author written evidence for inquiry on Scientific Publication by Science and Technology Committee, UK House of Commons. This evidence analyses the state of affairs in Alzheimer's disease (AD) research, concludes on "editorial and publisher corruption" by the major general science and neuroscience journals, and serves the basis for a referring the major conflict of interest in the field of AD for UK Serious Fraud Office investigation. The letter invites The President to lead the task to correct the situation and to help to restore integrity of science at all stages of scientific process.

Author: Alexei R. Koudinov
Authors Institution: Russian Academy of Medical Sciences, c/o P.O.Box 1665, Rehovot 76100 Israel, alexeikoudinov[at]neurobiologyoflipids.org

Key words: Alzheimer's disease; Niemann Pick type C disease; NPC; Potamkin prize; institutional corruption in medicine; public interest; public health; ethics; behavior; non disclosure; competing financial interest; Administration; scientific integrity; political; appointment; faculty; university; policymaking

Induction of cholesterol efflux in the CNS

Citation: Rebeck WG. Induction of cholesterol efflux in the CNS. Neurobiol Lipids Vol. 3, 1 (29 Feb 2004). Available at: http://neurobiologyoflipids.org/content/3/1/

Abstract: Intricate cellular mechanisms exist for maintaining proper cholesterol levels. Several recent studies of removal of excess cholesterol in the CNS have focused on the ABC-A1 lipid transporter and its regulation via the LXR nuclear hormone receptor. Cellular cholesterol is hydroxylated to form oxysterols (24-hydroxycholesterol in the brain), which bind LXR and promote gene transcription. LXR activation increases levels of ABC-A1 and apoE, which together act to remove cholesterol and other lipids from cells. Recent studies including Liang et al. suggest manipulation of the LXR system alters brain cholesterol homeostasis and apoE levels, and thus could be beneficial in approaches to Alzheimer disease therapeutics.

Author: G. William Rebeck
Authors Institution: Department of Neuroscience, Georgetown University, 3970 Reservoir Rd, NW, Washington, DC 20057-1464 USA

Key words: apolipoprotein; apoE; ABC-A1; LXR; oxysterols; Alzheimer's disease; cholesterol homeostasis efflux; neurodegeneration; lipoprotein; apolipoprotein; LRP; Down' syndrome; ApoE4; HMGCoA reductase; lipids; LDLr; LRP receptor; injury; Niemann Pick C (NPC)

33rd Society for Neuroscience annual meeting neurobiology of lipids sessions 2003

Citation: Editorial Material. 33rd Society for Neuroscience annual meeting neurobiology of lipids sessions 2003. Neurobiol Lipids Vol. 2, 3 (1 Oct 2003). Available at: http://neurobiologyoflipids.org/content/2/3/

Abstract: This article alerts interested readers about neurobiology of lipids sessions of the 33rd Society for Neuroscience (SfN) annual meeting, 8-12 November, 2003, New Orleans, LA. The abstracts were retrieved from the SfN web based abstract system as a result of the search for the key words cholesterol, phospholipid, lipoprotein, apolipoprotein, fatty acid, lipid, lipid peroxidation in abstract title/key words, abstract text or session title. The reference to each abstract entry includes day/time, program number, presentation type, location, authors list, first author first affiliation, and the abstract title. Each abstract title provides link to abstract text at the scholarone.com web site. The presented list yielded editors' choice short list of twenty noteworthy presentations. The short listed abstracts were invited to publish proceedings and lay language articles at the Neurobiology of Lipids.

Author: Editorial Material
Authors Institution: Neurobiology of Lipids, P.O.Box 1665 Rehovot 76100, Israel; sfnabstracts[at]neurobiologyoflipids.org

Key words: neuroscience of lipids; literature update; cholesterol; fatty acids; FA; SREBP; LXR; phospholipids; lipoprotein; lipid peroxidation; psychiatry; neurology

Polymorphisms in genes of proteins involved in cholesterol metabolism: evidence for Alzheimer's disease?

Citation: Kцlsch H. Polymorphisms in genes of proteins involved in cholesterol metabolism: evidence for Alzheimer's disease? Neurobiol Lipids Vol. 2, 2 (2 April 2003). Available at: http://neurobiologyoflipids.org/content/2/2/

Abstract: Cholesterol is suggested to be involved in the pathogenesis of Alzheimer's disease (AD). This commentary discusses the relevance of the polymorphisms in genes involved in cholesterol metabolism for the risk of AD, and explains why greater number of and larger studies are needed to provide solid evidence on whether such genes are involved in the pathogenesis of the disease.

Authors:Heike Kцlsch
Authors Institution: Department of Psychiatry, University of Bonn, Sigmund-Freud-Strasse 25, 53105 Bonn, Germany; email: Heike.Koelsch[at]ukb.uni-bonn.de

Key words: view point; commentary; cholesterol homeostasis; 24S-hydroxycholesterol; 24S-hydroxylase; CYP46; HMG-CoA reductase; neurodegeneration; lipoprotein; apolipoprotein; ApoE4; lipids; LRP receptor; Lp(a); gene ploymorphism; ABCA1

A link between cholesterol, CNS, synapse and brain diseases: is there a need for a reinvention?

Citation: Koudinov AR. A link between cholesterol, CNS, synapse and brain diseases: is there a need for a reinvention? Neurobiol Lipids Vol. 2, 1 (2 April 2003). Available at: http://neurobiologyoflipids.org/content/2/1/

Abstract: Since 1987 we know that "apolipoprotein E-containing lipoproteins may function to redistribute lipid and regulate cholesterol homeostasis within the brain". In 1993 we learned about the importance of "cholesterol synthesis and lipoprotein reuptake during synaptic remodeling". Over the past decade this knowledge was amassed (thanks to the pivotal contribution by many scientists) and elucidated the role for the failure of cholesterol homeostasis proper in neuronal degeneration. Still many questions remain. However, the statement that "a breakdown of cholesterol homeostasis may also play a role in neurodegenerative processes that have not been associated with this lipid so far" seems outdated.

Authors:Alexei R. Koudinov
Authors Institution: Russian Academy Med Sci, Moscow, Russian Federation, c/o P.O.Box 1665, Rehovot 76100 Israel, email: alexei[at]koudinov.info

Key words: cholesterol homeostasis; neurodegeneration; lipoprotein; apolipoprotein; LRP; Down's syndrome; ApoE4; electrophysiology; HMG CoA reductase; hippocampus; hippocampal slices; lipids; LDL; LDLR; VLDLR; LRP receptor; LTP; long term potentiation; lipid; Niemann Pick type C (NPC) disease; plasticity; memory

Editor's choice neurobiology of lipids sessions at Neuroscience 2004

Citation: Editorial material. Editor's choice neurobiology of lipids sessions at Neuroscience 2004. Neurobiol Lipids Vol. 1, 9 (22 March 2004). Available at: http://neurobiologyoflipids.org/content/1/9/

Abstract: This article alerts interested readers about editors’ choice neurobiology of lipids sessions of the 32nd Society for Neuroscience (SfN) Annual Meeting, 2-7 November, 2002, Orlando, Fla. The article quotes original Neuroscience 2002 abstracts, provides the references for proceedings articles (published in Neurobiology of Lipids and elsewhere) and related bibliography. The entire collection of the neurobiology of lipids sessions at Neuroscience 2002 is available as earlier Neurobiology of Lipids publication ( 2002, Vol. 1, 5, http://neurobiologyoflipids.org/content/1/5 ).

Authors:Editorial material
Authors Institution: Neurobiology of Lipids, P.O.Box 1665 Rehovot 76100, Israel, sfnabstracts[at]neurobiologyoflipids.org

Key words: neuroscience of lipids; literature update; cholesterol; fatty acids; fa; srebp; lxr; phospholipids; lipoprotein; lipid peroxidation; psychiatry; neurology; receptor; amyloid hypothesis; Alzheimer's disease; Down syndrome; synapse; synaptic plasticity

Alzheimer's amyloid beta protein restores brain function: a central role for cholesterol?

Citation: Koudinov AR, Koudinova NV. Amyloid beta protein restores hippocampal long term potentiation: a central role for cholesterol? Neurobiol Lipids Vol. 1, 8 (15 Sep 2003). Available at: http://neurobiologyoflipids.org/content/1/8/

Abstract: There is no understanding of the role of amyloid beta protein (Ab or Abeta) in brain function and Alzheimer's disease. In the present study we attempted to dissect out the role for Abeta in the synaptic plasticity in adult rat ex vivo hippocampal slices. The prolonged incubation of slices in our experimental setting preserved basic synaptic physiology but abrogated tetanus induced long term potentiation (LTP). Peptide Abeta1-40 rescued LTP while cholesterol synthesis inhibition abolished the restorative action of the peptide. Our observation confirms that Abeta protein is a functional player in cholesterol neurochemical pathways and in synaptic structure-functional plasticity. The finding also supports our proposed hypothesis that the change in Abeta biochemistry in Alzheimer's disease is a functional phenomenon aiming to compensate impaired cholesterol dynamics and associated neurotransmission and synaptic plasticity failure.

Authors:Alexei R. Koudinov and Natalia V. Koudinova
Authors Institution: Russian Academy of Medical Sciences, Moscow, Russian Federation, c/o P.O.Box 1665, Rehovot 76100 Israel, alexei[at]koudinov.info

Key words: Alzheimer's disease; amyloid precursor protein; APP; Down syndrome; etiology; lipids; learning; memory; long-term potentiation; LTP; LRP; neurodegeneration; oxidative stress; anti oxidation; PHF; NFT; tau; plaques; phospholipids; secretase; synapse; synaptic plasticity; SREBP; statins; Liver X LXR; sensor; presenilin

Abnormal cholesterol processing in Alzheimer's disease patient's fibroblasts

Citation: Dufour F et al. Abnormal cholesterol processing in Alzheimer's disease patient's fibroblasts. Neurobiol Lipids Vol. 1, 7 (14 March 2003). Available at: http://neurobiologyoflipids.org/content/1/7/

Abstract: Cholesterol has recently received attention as a potentially important factor in Alzheimer's disease (AD) etiology. Caveolin, which binds cholesterol, plays a prominent role in cellular cholesterol transport. Here, we found a higher level of cholesterol and caveolin in the caveolae-enriched fractions prepared from AD patients' fibroblasts compared with age and sex matched controls (AC). Furthermore, the cross-linking activation of the prion protein, which is known to link to signal transduction of caveolin, is altered in AD fibroblasts. Our results suggest a dysregulation of cholesterol processing in AD fibroblasts which may contribute to the pathogenesis of AD.

Authors:Franck Dufour and colleagues
Authors Institution: Blanchette Rockefeller Neurosciences Institute, 9601 Medical Center Drive, Rockville, MD 20850, USA, fdufour[at]brni-jhu.org

Key words: Alzheimer's disease; amyloid beta precursor; APP; Down syndrome; etiology; lipids; lipoprotein; neurodegeneration marker; secretase; caveolin; caveolae; membrane; cell culture; human; non-neuronal tissue; neurodegenerative disease; signal transduction; prion; PKC; cross-linking; fractioning; biochemistry; triton

Amyloid beta, neural lipids, cholesterol and Alzheimer's disease

Citation: Koudinova NV et al. Amyloid beta, neural lipids, cholesterol and Alzheimer's disease. Neurobiol Lipids Vol. 1, 6 (3 March 2003). Available at: http://neurobiologyoflipids.org/content/1/6/

Abstract: To date great number of articles were devoted to cholesterol (chol) but only few articles studied the role for chol in neuron function/degeneration. For decades this molecule had been known to be important for atherosclerosis and heart disease. First indication of the involvement of chol in Alzheimer disease (AD), however, come from the mid 1990s. At that time it was shown that heart disease patients develop brain deposits of amyloid beta (Ab or Abeta), a major dogmatic molecule of AD; that apoE (a chol transport apolipoprotein) allele e4 is a major genetic risk factor for AD; and that lab animals fed a chol diet express brain amyloid. These days it turns out that Abeta, long thought to be exclusively a pathologic protein, is a normal and functional apolipoprotein constituent of high density lipoproteins in plasma and CSF. Thus, we and others showed that Abeta modulates chol and phospholipid synthesis, and affects chol esterification. Protection of lipoproteins and other biomolecules from oxidation may represent another important function of Ab. We also discovered that neuronal chol homeostasis failure and the lack of chol supply to neurons by means of lipoprotein transport causes AD features, such as the failure of the neurotransmission and synaptic plasticity, degeneration of neuronal cell processes, and tau protein pathology.

Authors:Natalia V. Koudinova and colleagues
Authors Institution: Weizmann Institute of Science, Neurobiology/Biological Regulation, Candiotti Bldg, Rehovot 76100, Israel, nataliakoudinova[at]neurobiologyoflipids.org

Key words: Alzheimer's disease; amyloid beta precursor; APP; cytoskeleton; Down syndrome; etiology; lipids; learning; memory; lipoprotein; HDL; LDL; CSF; receptor; LTP; neurodegeneration marker; metal; oxidative stress; anti oxidation; PHF; NFT; tau phosphorylation; phospholipids; secretase; synaptic plasticity; SREBP; therapy; presenilin

32nd Society for Neuroscience annual meeting neurobiology of lipids sessions 2002

Citation: Editorial Material. 32nd Society for Neuroscience annual meeting neurobiology of lipids sessions 2002. Neurobiol Lipids Vol. 1, 5 (23 Sep 2002). Available at: http://neurobiologyoflipids.org/content/1/5/

Abstract: 32nd Society for Neuroscience Neurobiology of Lipids sessions' article alerts interested readers about the abstracts on the journal scope that were presented at the 32nd Society for Neuroscience (SFN) annual meeting, 2-7 November, 2002 in Orlando, Fla. The abstracts were retrieved from the SFN web based abstract system as a result of the 'abstract text' search for the key words cholesterol, phospholipids, lipoprotein, fatty acids, lipid and lipid peroxidation. The reference to each abstract entry includes day/time, program number, presentation type, location, authors list, first author first affiliation, and the abstract title. Each abstract title provides link to abstract text at the www.scholarone.com web site. The presented list yielded editors' choice short list of eighteen noteworthy presentations. The short listed abstracts/presentations were invited to publish proceedings articles at the Neurobiology of Lipids.

Author: Editorial Material
Authors Institution: Neurobiology of Lipids, P.O.Box 1665 Rehovot 76100, Israel; sfnabstracts[at]neurobiologyoflipids.org

Key words: neuroscience of lipids; literature update; cholesterol; fatty acids; FA; SREBP; LXR; phospholipids; lipoprotein; lipid peroxidation; psychiatry; neurology

Cholesterol and Alzheimer's disease

Citation: Wood GW et al. Cholesterol and Alzheimer's disease. Neurobiol Lipids Vol. 1, 3 (30 Aug 2002). Available at: http://neurobiologyoflipids.org/content/1/4/

Abstract: July 26, 2002 featured the conference "Cholesterol and Alzheimer's disease" held at the Biocenter, Frankfurt University, Frankfurt/Maine, Germany. The conference program included ten lectures and eight poster presentations on different aspects of the possible role for cholesterol in Alzheimer's disease and cholesterol neurobiology. This truly international round table event did not aim to come to the consensus but rather to summarize the advances and to discuss directions for near future development. This article presents the abstracts and related bibliography and aims to introduce readers to the multifarious subject of neural cholesterol with special emphasis on Alzheimer's disease and related disorders.

Authors: W. Gibson Wood and colleagues
Authors Institution: c/o Neurobiology of Lipids, P.O. Box 1665 Rehovot 76100, Israel; email: cholesterolandalzheimer[at]neurobiologyoflipids.org

Key words: treatment; cell biology; ABCA1; ApoE4; LRP; LDLR; apolipoprotein; phospholipid; amyloid beta precursor protein; alpha and beta secretase; aggregation and fibril formation; association study; PHF NFT tau phosphorylation; membrane fluidity; statin

The prion protein and cellular cholesterol homeostasis

Citation: Diomede L et al. The prion protein and cellular cholesterol homeostasis. Neurobiol Lipids Vol. 1, 3 (30 Nov 2002). Available at: http://neurobiologyoflipids.org/content/1/3/

Abstract: The amount of lipids in cell membranes seems to regulate the interaction of the prion protein with cells and the propagation of prions. We investigated how the synthetic human prion peptide PrP 106-126 affected the chemico-physical and biochemical properties of nerve and HL60 cells. PrP 106-126 rapidly increased cell membrane microviscosity, inhibited cellular cholesterol release and increased membrane cholesterol content. PrP also inhibited cellular 3-hydroxy-3-methylglutaryl-coenzyme A reductase activity. These findings indicate that PrP 106-126 alters cellular cholesterol homeostasis and may help clarify how changes in membrane lipid composition are involved in the progression of prion encephalopathies.

Authors: Luisa Diomede and colleagues
Authors Institution: Department of Molecular Biochemistry and Pharmacology and Department of Neurochemistry, Istituto di Ricerche Farmacologiche Mario Negri Via Eritrea 62, 20157 Milano, Italy; email: diomede[at]marionegri.it

Key words: Prion protein; PrP 106-126; 3-hydroxy-3-methylglutaryl-coenzyme A (HMG CoA) reductase; membrane fluidity; cell homeoviscosity; etiology; lipids; learning; memory; lipoprotein; receptor; LTP; neurodegeneration marker; oxidative stress; PHF NFT tau phosphorylation; phospholipids; synaptic plasticity; disease; therapy; nutrition; cytoskeleton; Down syndrome; prions; scrapie

Neurobiology of lipids opening note

Citation: Yehuda S. Neurobiology of lipids opening note. Neurobiol Lipids Vol. 1, 2 (15 July 2002). Available at: http://neurobiologyoflipids.org/content/1/2/

Abstract: The number of studies and scientific papers, which can be classified as related to the general area of neurobiology of lipids, has constantly grown during years. The "popularity" of the field is based not only on new technology and research tools, but also on the emergence of new theoretical avenues.

Author: Shlomo Yehuda
Authors Institution: Psychopharmacology Lab., Bar Ilan University, Ramat Gan 52900, Israel email: yehudas[at]mail.biu.ac.il

Key words: fatty acids; PUFA; cytoskeleton; etiology; lipids; learning; memory; lipoprotein; receptor; LTP; neurodegeneration marker; oxidative stress; PHF NFT tau phosphorylation; phospholipids; secretase; synaptic plasticity; SREBP; therapy; pathology; disease; nutrition; amyloid; precursor

The emerging neurobiology of cholesterol

Citation: Simmonds MA. The emerging neurobiology of cholesterol. Neurobiol Lipids Vol. 1, 1 (10 July 2002). Available at: http://neurobiologyoflipids.org/content/1/1/

Abstract: Although cholesterol gets a bad press as a cause of vascular disease, it is, of course, an essential component of all mammalian cells. In neurobiology, three quite different roles of cholesterol can be discerned: as a structural component of the plasma membranes of neurones and glia; as the precursor for a cascade of steroidal hormones and mediators affecting both genomic and non-genomic processes in neurones; and as a direct modulator of the functions of certain plasma membrane proteins.

Author: Mike A Simmonds
Authors Institution: Department of Pharmacology, School of Pharmacy, 29/39 Brunswick Square London WC1N 1AX UK, mikesimmonds@neurobiologyoflipids.org

Key words: Alzheimer; Alzheimer's disease; amyloid beta precursor; cytoskeleton; Down syndrome; etiology; lipids; learning; memory; lipoprotein; receptor; LTP; neurodegeneration marker; oxidative stress; PHF NFT tau phosphorylation; phospholipids; secretase; synaptic plasticity; SREBP; therapy