ratio, which is an important indicator of gene transcriptionactivation.Multiscale volume microscopy techniques and protocolsestablished for cellular microanatomy studies complementconventional 3D neuroimaging data on micro and nanoscale,and may well bridge the gap between ``cellular'' and ``circuit''levels in structural brain studies.

http://dx.doi.org/10.1016/j.npbr.2014.01.170

Marine bioactive products in the treatment of depressionand reduction of inflammation

C. Song

Research Institute for Marine Nutrition and Drugs, GuangdongOcean University, Zhanjiang, China

Oceans, occupying 80% of the earth, contain rich resource ofunique plants and animals, from which many bioactivecompounds with medical effects have been extracted. Unsa-turated omega-3 fatty acids eicosapentaenoic acid (EPA) anddocosahexanoic acid (DHA) are popularly used to treatdepression due to their effects of anti-inflammation andneuroprotection. However, EPA and DHA at different ratiosoften exert totally different therapeutical effects on depres-sion. Recent evidence shows that EPA and DHA may playdifferent roles in membrane incorporation, modulation ofgene expressions, activation of signaling pathways, andmetabolite formation. It suggests that there may be futureopportunity to refine recommendations for intake of individ-ual n-3 fatty acids according to clinical conditions.Except forn-3 fatty acids,marinepeptidesorproteinshavebeenshown to modulate neuroimmune interaction. In a beta-amyloid-induced cellular model, protein extractions fromshrimp sludge restored cell viability, largely reduced tumournecrosis factor (TNF)-a and interleukin (IL)-1b expressions,which associated with increased expression of neurotrophins.The treatment also significantly down-regulated apoptosisrelated genes.Another product, aplysinopsins are tryptophan-derived prod-ucts that have been isolated from a variety of marineorganisms and demonstrated a high affinity for the 5-HT2Band 5-HT2C receptor subtypes, with selectivity for 5-HT2B over5-HT2C. In the chick anxiety-depression model, some of itscompounds showed a modest antidepressant effect. As well,brominated indole alkaloids, a common class of metabolitesreported from sponges of the order Verongida have beenreported to have similar effects as desipramine and SSRIs inthe force swimming test. Extractions from similar marinesponge aplysina fistularis show anti-inflammatory activity inLPS-stimulated macrophages.These results may suggest that marine bioactive products arepotential candidates for reducing inflammation and treatingof depression.

http://dx.doi.org/10.1016/j.npbr.2014.01.171

Are antineuronal antibodies against NMDA receptorspotentially relevant in schizophrenia?

J. Steiner a,*, B. Bogerts a, W. Stoecker b

aDepartment of Psychiatry, University of Magdeburg, Germanyb Institute of Experimental Immunology, EUROIMMUN, Lübeck,Germany*Corresponding author.

Introduction: Evidence for symptomatic convergence of schiz-ophrenia and N-methyl-D-aspartate glutamate receptor(NMDA-R) encephalitis highlights the need for an assessmentof antibody prevalence and specificity for distinct diseasemechanisms in patients with a diagnosis of schizophreniaamong glutamatergic pathophysiologic abnormalities in psy-chiatric disorders.Methods: Serum from 459 patients admitted with acuteschizophrenia, major depression (MD), and borderline person-ality disorder (BLPD) or individuals serving as matchedcontrols was obtained from our scientific blood bank. Toexplore epitope specificity and antibody subtype, IgA/IgG/IgMNMDA-R (NR1a or NR1a/NR2b) and alpha-amino-3-hydroxyl-5-methyl-4-isoxazole-propionate receptors (AMPA-R) (GluR1/GluR2) serum antibodies were determined. Two hundredthirty matched healthy controls were compared with patients(unmedicated for at least 6 weeks) with schizophrenia(n = 121), MD (n = 70), or BLPD (n = 38).Results: Diverse NMDA-R antibodies were identified in 15subjects, primarily those with an initial schizophreniadiagnosis (9.9%), opposed to MD (2.8%), BLPD (0), and controls(0.4%). Retrospectively, 2 patients initially classified as havingcatatonic or disorganized schizophrenia were reclassified ashaving misdiagnosed NMDA-R encephalitis (presence ofspecific serum and cerebrospinal fluid IgG NR1a antibodies).In all other seropositive cases, the antibodies consisted ofclasses IgA and/or IgM or were directed against NR1a/NR2b(not against NR1a alone). None of the patients or controls hadantibodies against AMPA-R.Discussion: In conclusion, acutely ill patients with an initialschizophrenia diagnosis show an increased prevalence ofNMDA-R antibodies. The repertoire of antibody subtypes inschizophrenia and MD is different from that with NMDA-Rencephalitis. The latter disorder should be considered as adifferential diagnosis, particularly in young femaleswith acutedisorganized behavior or catatonia.

http://dx.doi.org/10.1016/j.npbr.2014.01.172

Mechanisms of passive vaccination against amyloidb-protein in APP23 mice

D.R. Thal a,*, J. Steinmetz a, I. Kosterin a, D. Abramowski b,J. Reichwald b, M. Fändrich c, M. Staufenbiel b, A.R. Upadhaya a

a Laboratory of Neuropathology – Institute of Pathology, Center forBiomedical Research, University of Ulm, Ulm, GermanybNovartis Institutes for Biomedical Research, Novartis Pharma AG,Basel, Switzerlandc Institute for Pharmaceutical Biotechnology, Center for BiomedicalResearch, University of Ulm, Ulm, Germany*Corresponding author at: Laboratory of Neuropathology – Instituteof Pathology, Center for Biomedical Research, University of Ulm,Helmholtzstrasse 8/1, Ulm, Germany.E-mail address: dietmar.thal@uni-ulm.de

The deposition of the amyloid b-protein (Ab) is a pathologicalhallmark lesion of Alzheimer's disease (AD). Vaccinationagainst Ab was considered as a treatment strategy againstAD by clearing Ab from the brain. Although active as well aspassive anti-Ab immunization led to a reduction of stained Abplaques and to a cognitive improvement of amyloid precursorprotein (APP) transgenicmice, i.e.mousemodels for AD-relatedAb deposition, clinical trials in AD patients failed. However,even in AD patients there was a reduced number of plaquesdetected with antibodies against Ab. Possible reasons for thelacking success of anti-Ab immunization in human AD treat-ment are 1. the treatment is not curative butmay be protective,

n e u r o l o g y , p s y c h i a t r y and b r a i n r e s e a r c h 2 0 ( 2 0 1 4 ) 3 – 2 724