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PubMedDate not supplied

Docosahexaenoic acid, the aquatic diet, and hominin encephalization: difficulties in establishing evolutionary links.

Distinctive characteristics of modern humans, including language, tool manufacture and use, culture, and behavioral plasticity, are linked to changes in the organization and size of the brain during hominin evolution. As brain tissue is metabolically and nutritionally costly to develop and maintain, early hominin encephalization has been linked to a release of energetic and nutritional constraints. One such nutrient-based approach has focused on the n-3 long-chained polyunsaturated fatty acid docosahexaenoic acid (DHA), which is a primary constituent of membrane phospholipids within the synaptic networks of the brain essential for optimal cognitive functioning. As biosynthesis of DHA from n-3 dietary precursors (alpha-linolenic acid, LNA) is relatively inefficient, it has been suggested that preformed DHA must have been an integral dietary constituent during evolution of the genus Homo to facilitate the growth and development of an encephalizing brain. Furthermore, preformed DHA has only been identified to an appreciable extent within aquatic resources (marine and freshwater), leading to speculation that hominin encephalization is linked specifically to access and consumption of aquatic resources. The key premise of this perspective is that biosynthesis of DHA from LNA is not only inefficient but also insufficient for the growth and maturation demands of an encephalized brain. However, this assumption is not well-supported, and much evidence instead suggests that consumption of LNA, available in a wider variety of sources within a number of terrestrial ecosystems, is sufficient for normal brain development and maintenance in modern humans and presumably our ancestors.

Animals↗
PubMed1997

Trypanosoma brucei brucei: a long-term model of human African trypanosomiasis in mice, meningo-encephalitis, astrocytosis, and neurological disorders.

The search for a chronic experimental model for human African trypanosomiasis (HAT) in animals with cerebral lesions and neurological disorders has been difficult. Models with meningo-encephalitis have been proposed using Trypanosoma brucei gambiense or T. b. rhodesiense. Meningo-encephalitis is rare in infection with T. b. brucei. It has been shown that the treatment of mice infected with T. b. brucei with diminazene aceturate (Berenyl) led to development of a rapid meningo-encephalitis. In this study, we report the development of a chronic experimental model of HAT in mice infected with T. b. brucei AnTat 1.1E. To obtain a chronic evolution of the infection, on Day 21 postinfection, mice were treated with a dose of suramin (Moranyl) at 20 mg x kg(-1) body weight, a dose which failed to eliminate trypanosomes in the central nervous system (CNS). This treatment, repeated after each parasitemic relapse in the blood, allowed animals to survive more than 300 days postinfection. After a few weeks of infection, mice displayed neurological signs. Histological studies showed the appearance of increasing inflammatory lesions, from meningitis to meningo-encephalitis, with progression of lesions throughout the perivascular spaces in cerebral and cerebellum parenchyma. No demyelination or neuronal alteration were observed except in the necrotic spaces. Trypanosomes were observed in different structures in CNS. An immunohistochemical study of glial fibrillary acidic protein (GFAP) showed an increasing astrocytosis according to the duration of the infection. This model reproduces neurological and histological pathology observed in the human disease and can be useful for further immunopathological, neurohistological and therapeutic studies on this condition.

Animals↗
PubMed1993

Immunogens of encephalitis viruses.

The equine encephalitis viruses are members of the genus Alphavirus, in the family Togaviridae. Three main virus serogroups represented by western (WEE), eastern (EEE) and Venezuelan equine encephalitis (VEE) viruses cause epizootic and enzootic infection of horses throughout the western hemisphere. All equine encephalitis viruses are transmitted through the bite of an infected mosquito. The first equine encephalitis virus vaccines were produced by virus inactivation. Problems with inadequate inactivation, which may have caused a major epidemic/epizootic of VEE in central America and Texas in the 1970s, led to the development of a live attenuated VEE virus vaccine (TC-83) derived by cell culture passage. Inactivated vaccines are still used to prevent equine infections with WEE and EEE viruses. Alphaviruses are small single stranded, positive sense RNA viruses. The 12000 nucleotide genome is enclosed in an icosahedral nucleocapsid composed of multiple copies of the capsid (C) protein. The virion is enveloped. The membrane is modified by the insertion of heterodimers of two glycoproteins: E1 and E2. Monoclonal antibody analysis of the surface glycoproteins have provided a detailed understanding of important protective antigens. Recent studies comparing gene sequences from virulent and avirulent VEE viruses have begun to delineate mechanisms of alphavirus attenuation.

Alphavirus↗
PubMed2005

Human encephalization and developmental timing.

Human evolution is frequently analyzed in the light of changes in developmental timing. Encephalization in particular has been frequently linked to the slow pace of development in Homo sapiens. The "brain allometry extension" theory postulates that the progressive extension of a conserved primate brain allometry into postnatal life was the basis for brain enlargement in the human lineage. This study shows that published primate and human growth data do not corroborate this model. Instead, the unique encephalization of H. sapiens is alternatively described as the result of evolutionary changes in three aspects of developmental timing. The first is a moderate extension in the duration of brain growth relative to our closest extant relatives, contrary to the view that human brain growth is drastically prolonged into postnatal life. Second, humans evolved a derived brain allometry in comparison with chimpanzees and early hominins. Third, humans (and other anthropoid primates to a lesser degree) display a significant retardation in early postnatal body growth in comparison with other mammals, which directly affects adult encephalization in our species. The rejection of the "brain allometry extension" model may require a reevaluation of the adaptive scenarios proposed to explain how human encephalization evolved.

Animals↗
PubMed2005

BR serine/threonine kinase 2: a new autoantigen in paraneoplastic limbic encephalitis.

We describe a new antigen, BR serine/threonine kinase 2 (BRSK2), identified by an antibody present in the serum of a patient with limbic encephalitis and small-cell lung cancer (SCLC). Patient's serum immunolabeled the neuronal cytoplasm and, less intense, the neuropil of rat brain but did not immunoreact with other rat tissues with the exception of testis. Immunoblots of rat brain homogenate identified several immunoreactive bands in the range of 88-82 kDa and a weaker broad band of 47-43 kDa. Probing a rat hippocampus expression library with the patient's serum resulted in the isolation of BR serine/threonine kinase 2 (BRSK2), a protein (also know as SAD1B kinase) preferentially expressed in the brain and testis and implicated in neuronal polarization as well as synaptic development. Eluted IgG from the BRSK2 clone gave a similar immunolabeling than the patient's serum by immunohistochemistry and immunoblot of rat brain and testis. BRSK2 antibodies reacted with two SCLC from patients without paraneoplastic neurological syndromes. No anti-BRSK2 antibodies were found in the serum of 50 patients with SCLC without PNS, 19 with limbic encephalitis without onconeural antibodies, 50 with anti-Hu antibodies and several paraneoplastic neurological syndromes, including 14 with limbic encephalitis, and 160 with a variety of non-paraneoplastic neurological syndromes. Our study suggests BRSK2 may be an autoantigen involved in the pathogenesis of SCLC-associated limbic encephalitis.

Antibody Affinity↗
PubMed2004

[The presentation of small-cell lung cancer with metastatic carcinomatous encephalitis in a non-Hodgkin's lymphoma patient].

BACKGROUND: Carcinomatous encephalitis or milary cerebral metastases characterized by signs of diffuse encephalopathy is a rare form of brain metastases. Tiny tumor nodules are seen throughout the cortical and subcortical gray matter. OBSERVATION: We report the case of a patient with a history of non-Hodgkin lymphoma who developed carcinomatous encephalitis probably secondary to small-cell lung cancer. This case is discussed in light of findings of 16 cases of carcinomatous encephalitis reported in the literature. We discuss clinical, radiological, histological, pathophysiological characteristics and the survival of this form. CONCLUSION: The frequency of carcinomatous encephalitis is underestimated because clinical expression is non specific. Brain magnetic resonance imaging must be performed in all patients presenting encephalopathy without an obvious cause.

Aged↗
PubMed2004

Exocytosis and Fas mediated cytolytic mechanisms exert protection from West Nile virus induced encephalitis in mice.

Infection of mice with the flaviviruses West Nile virus (WNV) and Murray Valley encephalitis (MVE) induces cytolytic T-cell responses which are highly cross-reactive on target cells infected with heterologous flaviviruses. Of C57BL/6 mice infected with low doses (10(2)-10(6) PFU) of either virus, 30-40% develop encephalitis and die within 10-12 days. Mice with defects in the Fas or granule exocytosis (perforin and granzymes A and B) pathway of cellular cytotoxicity display reduced mortality and increased survival time when infected with MVE and are protected from encephalitis when deficient in both pathways. This contrasts with infection with WNV where defects in these cytolytic mechanisms increase the percentage of mice that succumb to encephalitis. Thus, no generalizations as to protective or detrimental effects of cytolytic effector functions in recovery from closely related flavivirus infections can be made. Virus-host immune interactions have to be assessed individually and cannot be generalized.

Animals↗
PubMed2004

An occipital lobe epileptogenic focus in a patient with West Nile encephalitis.

Although most human cases of West Nile (WN) fever are benign, approximately 1% produce severe neurological illness. Meningitis and/or encephalitis comprise 75% of hospitalized cases with seizures in 10-15%. Occipital lobe seizures, often mimicking other primary seizure types due to extra-occipital spread, is uncommon in adults and especially so from an infectious origin. A case of WN encephalitis presenting with a simple partial seizure, focal motor, resulting from an occipital epileptogenic focus is reported. The atypical epileptogenic location of the case and the observed frequency of seizures in WN encephalitis suggest that this virus is particularly irritative to cortical neuronal networks. Thus when seizures especially with atypical EEG patterns present during an acute febrile illness in the warmer months, WN encephalitis should be considered.

Aged↗
PubMed1992

Relationship of cerebrospinal fluid immune activation associated factors to HIV encephalitis.

OBJECTIVES AND DESIGN: Because macrophages are the predominant immune cell and the predominant infected cell in the brains of patients with HIV encephalitis, we studied macrophage and immune activation-associated factors in the cerebrospinal fluid (CSF) from 39 autopsied AIDS cases for whom complete neuropathologic evaluation of the brain was available. RESULTS: CSF HIV p24 antigen was present in less than one-third of cases (11 out of 39). Less than half of the autopsies with moderate to severe parenchymal infection by HIV had high levels of CSF p24, although all autopsies with elevated levels of HIV p24 had moderate to severe HIV encephalitis. Elevated levels of cytokines, beta 2-microglobulin, neopterin, and quinolinic acid were observed. CONCLUSIONS: Although many of the CSF findings showed a strong correlation with each other, none showed a strong correlation with the severity of HIV infection of the brain itself. The absence of a close association between CSF abnormalities and HIV encephalitis could reflect the abundance of complicating opportunistic infections in these terminally ill patients or the inadequacy of CSF as a marker of basal ganglia involvement in HIV encephalitis. These findings complicate interpretation of clinical studies of CSF in patients with AIDS where neuropathologic evaluation is unavailable.

AIDS Dementia Complex↗
PubMed1998

SCID mice with HIV encephalitis develop behavioral abnormalities.

Severe combined immunodeficient (SCID) mice inoculated intracerebrally (i.c.) with HIV-infected human monocytes develop brain pathology similar to that in humans with HIV encephalitis. This includes HIV-positive macrophages and multinucleated giant cells, astrogliosis, microglial nodules, and neuronal dropout. These xenografts survive about 1 month. To develop a model of chronic HIV encephalitis and to assay the resulting behavioral abnormalities, we reinoculated SCID mice i.c. every 4 weeks for 3 months with either HIV-infected human monocytes (n = 5) or uninfected human macrophages (n = 4) or administered no inoculation (n = 6); these three groups were monitored for behavioral abnormalities. Tests of cognitive function in a Morris water maze 3.5 months after the first inoculation suggested that HIV-infected mice performed poorly compared with controls. Following testing in the water maze on days 4 and 5 of acquisition, motor activity of infected mice was reduced in comparison with that of controls. Retention of goal location when tested 1 week later was impaired in HIV-infected mice compared with controls. Histopathologic analysis of brains revealed significant astrogliosis and strongly suggested higher numbers of major histocompatibility complex (MHC) class II-positive multinucleated macrophages in HIV-infected compared with control mice. Thus, our preliminary studies indicate that SCID mice with HIV encephalitis develop behavioral abnormalities reminiscent of human disease. These behavioral abnormalities are associated with significantly increased astrogliosis, the presence of HIV, and probably multinucleated giant cells. These studies further support the use of this SCID animal model system for studies of the pathogenesis of HIV encephalitis and for drug interventions.

AIDS Dementia Complex↗
PubMed1985

Animal intelligence as encephalization.

There is no consensus on the nature of animal intelligence despite a century of research, though recent work on cognitive capacities of dolphins and great apes seems to be on one right track. The most precise quantitative analyses have been of relative brain size, or structural encephalization, undertaken to find biological correlates of mind in animals. Encephalization and its evolution are remarkably orderly, and if the idea of intelligence were unknown it would have to be invented to explain encephalization. The scientific question is: what behaviour or dimensions of behaviour evolved when encephalization evolved? The answer: the relatively unusual behaviours that require increased neural information processing capacity, beyond that attributable to differences among species in body size. In this perspective, the different behaviours that depend on augmented processing capacity in different species are evidence of different intelligences (in the plural) that have evolved.

Adaptation, Biological↗
PubMed2006

CD8(+) T cell-mediated immune responses in West Nile virus (Sarafend strain) encephalitis are independent of gamma interferon.

The flavivirus West Nile virus (WNV) can cause fatal encephalitis in humans and mice. It has recently been demonstrated, in an experimental model using WNV strain Sarafend and C57BL/6 mice, that both virus- and immune-mediated pathology is involved in WNV encephalitis, with CD8(+) T cells being the dominant subpopulation of lymphocyte infiltrates in the brain. Here, the role of activated WNV-immune CD8(+) T cells in mouse WNV encephalitis was investigated further. Passive transfer of WNV-immune CD8(+) T cells reduced mortality significantly and prolonged survival times of mice infected with WNV. Early infiltration of WNV-immune CD8(+) T cells into infected brains is shown, suggesting a beneficial contribution of these lymphocytes to recovery from encephalitis. This antiviral function was not markedly mediated by gamma interferon (IFN-gamma), as a deficiency in IFN-gamma did not affect mortality to two strains of WNV (Sarafend and Kunjin) or brain virus titres significantly. The cytolytic potential, as well as precursor frequency, of WNV-immune CD8(+) T cells were not altered by the absence of IFN-gamma. This was reflected in transfer experiments of WNV-immune CD8(+) T cells from IFN-gamma(-/-) mice into WNV-infected wild-type mice, which showed that IFN-gamma-deficient T cells were as effective as those from WNV-immune wild-type mice in ameliorating disease outcome. It is speculated here that one of the pleiotropic functions of IFN-gamma is mimicked by WNV-Sarafend-mediated upregulation of cell-surface expression of major histocompatibility complex antigens, which may explain the lack of phenotype of IFN-gamma(-/-) mice in response to WNV.

Adoptive Transfer↗
PubMed1995

Activation of nuclear factor kappa B in brains from children with HIV-1 encephalitis.

Human immunodeficiency virus type 1 (HIV-1) infection of the central nervous system is associated with decreased neuronal density in discrete areas of the brain. Neuronal loss may occur via apoptosis, initiated by soluble neurotoxic factors secreted from HIV-1 infected macrophages and microglia. To examine further the molecular events involved in HIV-1 neuropathogenesis, we assessed the activity of NF kappa B, an inducible transcription factor involved in the activation of multiple proinflammatory, and potentially neurotoxic, genes. NF kappa B was analysed by immunocytochemistry using specific antisera to the NF kappa B p. 50 and p. 65 subunits. Brains from children with HIV-1 encephalitis and progressive encephalopathy were found to contain increased numbers of NF kappa B immunoreactive cells, relative to control brains (HIV-1 negative, or HIV-1 positive without encephalitis). Double-labelling studies using antibodies to CD68, or RCA-1 lectin, markers for cells of monocyte/macrophage lineage, revealed an increase in the number of microglia and macrophages with nuclear immunoreactivity for NF kappa B in association with HIV-1 encephalitis. NF kappa B positive multinucleated giant cells were also detected, as were cells which contained both NF kappa B and HIV-1 antigen. In contrast, the number of neurons and GFAP-positive astrocytes that were immunoreactive for NF kappa B was approximately the same in all groups of subjects. These data are consistent with the hypothesis that persistent, high-level activation of NF kappa B may promote the sustained production of neurotoxins by microglia and macrophages during HIV-1 encephalitis.

AIDS Dementia Complex↗
PubMed2001

The West Nile virus encephalitis outbreak in the United States (1999-2000): from Flushing, New York, to beyond its borders.

Viruses cause most forms of encephalitis. The two main types responsible for epidemic encephalitis are enteroviruses and arboviruses. The City of New York reports about 10 cases of encephalitis yearly. Establishing a diagnosis is often difficult. In August 1999, a cluster of five patients with fever, confusion, and weakness were admitted to a community hospital in Flushing, New York. Flaccid paralysis developed in four of the five patients, and they required ventilatory support. Three, less severe, cases presented later in the same month. An investigation was conducted by the NewYork City (NYC) and New York State (NYS) health departments and the national Centers for Disease Control and Prevention (CDC). The West Nile virus (WNV) was identified as the etiologic agent. WNV is an arthropod-borne flavivirus, with a geographic distribution in Africa, the Middle East, and southwestern Asia. It has also been isolated in Australia and sporadically in Europe but never in the Americas. The majority of people infected have no symptoms. Fever, severe myalgias, headache, conjunctivitis, lymphadenopathy, and a roseolar rash can occur. Rarely, encephalitis or meningitis is seen. The NYC outbreak resulted in the first cases of WNV infection in the Western Hemisphere and the first arboviral infection in NYC since yellow fever in the nineteenth century. The WNV is now a public health concern in the United States.

Disease Outbreaks↗
PubMed2002

Human brain parenchymal microglia express CD14 and CD45 and are productively infected by HIV-1 in HIV-1 encephalitis.

Microglia are endogenous brain macrophages that show distinct phenotypes such as expression of myeloid antigens, ramified morphology, and presence within the neural parenchyma. They play significant roles in a number of human CNS diseases including AIDS dementia. Together with monocyte-derived (perivascular) macrophages, microglia represent a major target of HIV-1 infection. However, a recent report challenged this notion based on findings in SIV encephalitis. This study concluded that perivascular macrophages can be distinguished from parenchymal microglial cells by their expression of CD14 and CD45, and that macrophages, but not microglia, are productively infected in SIV and HIV encephalitis. To address whether parenchymal microglia are productively infected in HIV encephalitis, we analyzed expression of CD14, CD45 and HIV-1 p24 in human brain. Microglia were identified based on their characteristic ramified morphology and location in the neural parenchyma. We found that parenchymal microglia are CD14+ (activated), CD45+ (resting and activated), and constitute approximately two thirds of the p24+ cells in HIV encephalitis cases. These results demonstrate that microglia are major targets of infection by HIV-1, and delineate possible differences between HIVE and SIVE. Because productively infected tissue macrophages serve as the major viral reservoir, these findings have important implications for AIDS.

AIDS Dementia Complex↗
PubMed1990

Severe encephalitis resulting from coinfections with HIV and JC virus.

We observed 3 cases of progressive multifocal leukoencephalopathy (PML) among frozen CNS samples obtained at autopsy from 102 adult AIDS patients. In 2 patients, PML was associated with severe HIV encephalitis. In those 2 cases, the areas of extensive JC-induced demyelination were massively infiltrated by HIV infected macrophages/microglial cells with evidence for localized increase of HIV encephalitis in PML lesions. Using immunohistochemistry and in situ hybridization, we demonstrated that each virus infects, in a latent or productive fashion, different CNS cell populations. Therefore, the extension of HIV encephalitis could not be related to an intracellular transactivation of 1 virus by the other. However, the results are consistent with dissemination of viral infection by the recruitment of HIV-infected macrophages to damaged areas of the brain. This phenomenon might be generalized to other pathogens that are frequently associated with HIV CNS infection. Early detection and treatment of opportunistic CNS lesions could be important to prevent extension of HIV encephalitis.

AIDS Dementia Complex↗
PubMed2003

Clinical signs as a guide for performing HSV-PCR in correct diagnosis of herpes simplex virus encephalitis.

BACKGROUND: Clinical criteria (symptoms) are not reliable enough to differentiate between different causes of encephalitis. The clinical presentation of herpes simplex virus encephalitis (HSVE) is not classically constant and in such a patient, therefore, it is vital to make early diagnosis. AIMS: To investigate satisfactory and crucial clinical signs as guide to perform HSV-PCR in a rapid diagnosis of herpes simplex virus encephalitis. MATERIAL AND METHODS: A total of 156 CSF specimens from 70 patients with clinically suspected HSVE or meningoencephalitis were tested. The criteria for cases suspected of HSVE were fever >380C, altered mental status and other critical manifestations. CSF features, irregularity in brain CT scan and MRI findings were also assessed. All the specimens were collected before and after Acyclovir treatment. Polymerase chain reaction was performed using primers, which amplified DNA sequences for both HSV-1 and HSV-2. STATISTICAL ANALYSIS: To analyze data, two-tailed Fisher's exact test and the X2-test with Yates' correction were used as appropriate. The odds ratio was used to express the strength of association between the clinical factors and the PCR results. RESULTS: HSV-DNA was detected in 18% of the specimens, belonging to 25.7% of the patients. Results indicate that the majority of the clinical symptoms are not specific to definitive clinical diagnosis of HSVE, except alteration in the level of consciousness--odds ratio [0.27 (0.07-0.96) (P=0.033)]; and lateralization sign--odds ratio [4.7 (0.98-22.6) (P=0.023)]. However, laboratory data, including total white blood cell count, especially the number of lymphocytes, and MRI findings could be suggested for HSV-PCR examination. CONCLUSION: At the first admission, a preliminary finding of at least two important clinical features mentioned above along with the pattern of CSF cell and differential counts could be sufficient to perform HSV-PCR which could ultimately result in a rapid and correct diagnosis of herpes simplex encephalitis.

Adolescent↗
PubMed1975

Encephalitis after administration of live measles vaccine.

In a previously well child with no evidence of pre-existing immunologic defect a fatal encephalitis developed 10 days after administration of measles vaccine. There was pathologic evidence of an early viral encephalitis characterized by perivascular mononulcear infiltrates. Although the virus was not recovered, the diagnosis of a measles virus infection and encephalitis is supported by the postmortem findings of Warthin-Finkeldey cells in lymphoid tissues, an intranuclear inclusion in the brain and histologic changes of encephalitis.

Autopsy↗