Autism and other related abstracts

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Neurobiol Dis 2002 Mar;9(2):107-25 Related Articles, Books, LinkOut

Genetic and immunologic considerations in autism.

Korvatska E, Van de Water J, Anders TF, Gershwin ME.

Division of Rheumatology, Allergy, and Clinical Immunology, University of

California at , , California, 95616

According to recent epidemiological surveys, autistic spectrum disorders

have become recognized as common childhood psychopathologies. These

life-lasting conditions demonstrate a strong genetic determinant consistent

with a polygenic mode of inheritance for which several autism susceptibility

regions have been identified. Parallel evidence of immune abnormalities in

autistic patients argues for an implication of the immune system in

pathogenesis. This review summarizes advances in the molecular genetics of

autism, as well as recently emerging concerns addressing the disease

incidence and triggering factors. The neurochemical and immunologic findings

are analyzed in the context of a neuroimmune hypothesis for autism. Studies

of disorders with established neuroimmune nature indicate multiple pathways

of the pathogenesis; herein, we discuss evidence of similar phenomena in

autism. ©2002 Elsevier Science (USA).

PMID: 11895365 [PubMed - in process]

Curr Opin Neurobiol 2002 Feb;12(1):115-8 Related Articles, Books, LinkOut

Maternal infection: window on neuroimmune interactions in fetal brain

development and mental illness.

PH.

Biology Division, California Institute of Technology, 91125, Pasadena,

California, USA

Direct viral infection of the developing brain can have disastrous

consequences for the fetus. More subtle and perhaps more insidious are viral

infections of the pregnant mother, which can have long-lasting effects such

as an increased risk of schizophrenia in the offspring. A recent mouse model

has shown that respiratory infection in the pregnant mother leads to marked

behavioral and pharmacological abnormalities in the offspring, some of which

are relevant for schizophrenia and autism. This effect on fetal brain

development might be caused by the maternal antiviral immune response,

possibly mediated by cytokines.

PMID: 11861174 [PubMed - in process]

Annu Rev Immunol 2002;20:125-63 Related Articles, Books, LinkOut

Neuroendocrine regulation of immunity.

Webster JI, Tonelli L, Sternberg EM.

Section on Neuroimmune Immunology and Behavior, National Institute of Mental

Health, Bldg 36, Room 1A 23 (MSC 4020), 36 Convent Drive, Bethesda, land

20892-4020; e-mail: jwebster@... tonellil@...

ems@...

A reciprocal regulation exists between the central nervous and immune

systems through which the CNS signals the immune system via hormonal and

neuronal pathways and the immune system signals the CNS through cytokines.

The primary hormonal pathway by which the CNS regulates the immune system is

the hypothalamic-pituitary-adrenal axis, through the hormones of the

neuroendocrine stress response. The sympathetic nervous system regulates the

function of the immune system primarily via adrenergic neurotransmitters

released through neuronal routes. Neuroendocrine regulation of immune

function is essential for survival during stress or infection and to

modulate immune responses in inflammatory disease. Glucocorticoids are the

main effector end point of this neuroendocrine system and, through the

glucocorticoid receptor, have multiple effects on immune cells and

molecules. This review focuses on the regulation of the immune response via

the neuroendocrine system. Particular details are presented on the effects

of interruptions of this regulatory loop at multiple levels in

predisposition and expression of immune diseases and on mechanisms of

glucocorticoid effects on immune cells and molecules.

PMID: 11861600 [PubMed - in process]

Mol Neurobiol 2001 Aug-Dec;24(1-3):183-99 Related Articles, Books, LinkOut

Nerve growth factor: a neurokine orchestrating neuroimmune-endocrine

functions.

Skaper SD.

Neurology Centre of Excellence for Drug Discovery, GlaxoKline

Pharmaceuticals, North, Harlow, Essex, UK. _Skaper-1@...

Nerve growth factor (NGF) is widely recognized as a target-derived factor

responsible for the survival and maintenance of the phenotype of specific

subsets of peripheral neurons and basal forebrain cholinergic nuclei during

development and maturation. Other NGF-responsive cells are now known to

belong to the hemopoietic-immune system and to populations in the brain

involved in neuroendocrine functions. The concentration of NGF is elevated

in a number of inflammatory and autoimmune states in conjunction with

increased accumulation of mast cells. Mast cells and NGF appear to be

involved in neuroimmune interactions and tissue inflammation. Mast cells

themselves are capable of producing and responding to NGF, suggesting that

alterations in mast cell behavior may trigger maladaptive neuroimmune tissue

responses, including those of an autoimmune nature. Moreover, NGF exerts a

modulatory role on sensory nociceptive nerve physiology in the adult, and

appears to correlate with hyperalgesic phenomena occurring in tissue

inflammation. NGF can thus be viewed as a multifactorial modulator of

neuroimmune-endocrine functions.

PMID: 11831552 [PubMed - in process]

neurotrophins: J Neurosci Res 2002 Jan 15;67(2):255-63 Related Articles,

Books, LinkOut

Effects of IL-1beta, IL-6 or LIF on rat sensory neurons co-cultured with

fibroblast-like cells.

Edoff K, Jerregard H.

Division of Cell Biology, Department of Biomedicine and Surgery, Faculty of

Health Sciences, University of Linkoping, Linkoping, Sweden.

Inflammation may affect the local presence of sensory nerve fibers in situ

and inflammatory mediators influence sensory neurons in vitro. In the

present study we have investigated effects of the cytokines

interleukin-1beta (IL-1beta, interleukin-6 (IL-6), and leukemia inhibitory

factor (LIF) on survival of and neurite growth from neonatal rat sensory

neurons co-cultured with fibroblast-like cells prepared from neonatal rat

skin (sFLCs) or perichondrium (pFLCs). The results showed that both FLC

types expressed receptors for all three cytokines. Five ng/ml of either

cytokine, but not lower or higher concentrations, supported survival of DRG

neurons co-cultured with sFLCs. Neuronal survival was also enhanced by

addition of the soluble IL-6 receptor (rsIL-6R) with or without IL-6. In

co-cultures with pFLCs neuronal survival was promoted by IL-6, increasing

with cytokine concentration. Addition of rsIL-6R without IL-6 did also

stimulate neuronal survival. The growth of neurites from DRG neurons

co-cultured with sFLCs was stimulated by 0.5 ng/ml LIF, unaffected by 5

ng/ml LIF and inhibited by 50 ng/ml LIF. Considering DRG neurons co-cultured

with pFLCs, 50 ng/ml of either of the three cytokines, as well as rsIL-6R

conditioned medium, stimulated neurite outgrowth. Some of the cytokine

effects observed were reduced by application of antibodies against nerve

growth factor (NGF). We conclude that that the cytokines examined affect DRG

neurons in terms of survival or neuritogenesis, that the effects are

influenced by cytokine concentration and the origin of the FLCs and that

some of the effects are indirect, probably being mediated by factors

released from FLCs. Copyright 2002 Wiley-Liss, Inc.

Vitam Horm 2002;64:185-219 Related Articles, Books, LinkOut

Interleukin-1 beta exerts a myriad of effects in the brain and in particular

in the hippocampus: analysis of some of these actions.

Lynch MA.

Trinity College Institute for Neuroscience and Department of Physiology,

Trinity College, Dublin 2, Ireland.

The realization, in the past decade or so, that bidirectional communication

between the central nervous system and the immune system was likely has

sparked an explosion of interest in the roles certain cytokines,

particularly the proinflammatory cytokine interleukin-1 beta (IL-1 beta),

might play in the brain. The observation that IL-1 type I receptor was

expressed in highest density in the hypothalamus was of significance in

identifying a role for IL-1 beta in neuroendocrine modulation. However, the

finding that receptor expression was also high in the hippocampus, an area

of the brain which plays a pivotal role in memory and learning, has led to

uncovering a role for IL-1 beta in cognitive function. There is now a great

deal of evidence suggesting that IL-1 beta plays a significant role in

hippocampal synaptic function, and the possibility that IL-1 beta may

trigger some of the detrimental changes in certain neurodegenerative

diseases is currently being assessed. The review addresses some of the

issues relating to the role of IL-1 beta in the brain, specifically in the

hippocampus.

PMID: 11898392 [PubMed - in process]

Expert Opin Ther Targets 2002 Feb;6(1):57-72 Related Articles, Books

Neuroendocrine influence on thymic haematopoiesis via the

reticulo-epithelial cellular network.

Bodey B.

Department of Pathology, Keck School of Medicine, University of Southern

California, Childrens Center for Cancer and Blood Diseases, Childrens

Hospital Los Angeles, Los Angeles, CA, USA. Bodey18@...

The thymus provides an optimal cellular and humoral microenvironment for a

cell line committed differentiation of haematopoietic stem cells. The

immigration process requires the secretion of at least one peptide, called

thymotaxin, by cells of the reticulo-epithelial (RE) network of the thymic

stromal cellular microenvironment. The thymic RE cells are functionally

specialised based on their intrathymic location and this differentiation is

modulated by various interaction signals of differentiating Thymocytes and

other nonlymphatic, haematopoietic stem cells. The subcapsular, endocrine,

RE cell layer is comprised of cells filled with periodic acid

Shiff's-positive granules, which also express A2B5/TE4 cell surface antigens

and MHC Class I (HLA A, B, C) molecules. Thymic nurse cells also produce

thymosins beta 3 and beta 4 and display a neuroendocrine cell specific

immunophenotype (IP): Thy-1+, A2B5+, TT+, TE4+, UJ13/A+, UJ127.11+,

UJ167.11+, UJ181.4+ and presence of common leukocyte antigen (CLA+).

Cortical RE cells express a surface antigen, gp200-MR6, which plays a

significant role of thymocyte differentiation. Medullar RE cells display MHC

Class II (HLA-DP, HLA-DQ, HLA-DR) molecule restriction. Thymic RE cells also

produce numerous cytokines that are important in various stages of

haematopoietic cell activation and differentiation. The co-existence of

pituitary hormone and neuropeptide secretion, as well as the production of a

number of interleukins and growth factors, and expression of receptors for

all, by RE cells is an unique molecular biological phenomenon. Thymic

neuroendocrine polypeptides are the source of self antigens presented by the

MHC molecules to differentiating haematopoietic stem cells. On the level of

individual RE cells, the numerous projections associated with a single cell,

which engulf developing lymphocytes, nurturing and guiding them in their

maturation, may differ in their hormone production and/or hormone receptor

expression profile, thus allowing a single cell to be involved in distinct,

separate steps of the T-cell and other haematopoietic cell maturation

process. Thymic RE cells represent an important cellular and humoural

network within the thymic microenvironment and are involved in the

homeopathic regulation mechanisms of the multicellular organism. The

intrathymic T-lymphocyte selection is a complex, multistep process,

influenced by several functionally specialised RE cells and under

immuno-neuroendocrine regulation control reflecting the dynamic changes of

the mammalian organism.

PMID: 11901481 [PubMed - in process]

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