NeuroImmunology

Beer has fueled a lot of bad ideas. But on a Friday afternoon in 2007, it helped two Alzheimer's researchers come up with a really a good one.

A new clinical trial indicates that stem cell transplants can prevent the progression of MS. The transplants also helped to improve the symptoms of patients.

Alemtuzumab is a humanized anti-CD52 monoclonal antibody approved in more than 65 countries for the treatment of relapsing–remitting multiple sclerosis (RRMS). Compared wit

The pathogenesis of multiple sclerosis (MS) has not been clarified. In addition to environmental factors; genetic determinants have been implicated in the pathogenesis of MS. Furthermore, endogenous retroviruses (ERV) might play a role in MS. The presence of oligoclonal immunoglobulin in cerebrospinal fluid (CSF) is a typical feature of MS. Recently, genetic polymorphisms in loci on human chromosomes 6, 14 and 18 have been identified as major determinants of CSF antibody levels in MS. The functional relevance of these single nucleotide polymorphisms (SNPs) remains unclear and none of them is located in an open reading frame. In previous studies, we identified ERV sequences in the vicinity of MS associated SNPs. Here, we describe the identification of ERV sequences in the neighborhood of SNPs associated with CSF antibody levels. All of the identified SNPs are located in the vicinity of ERV sequences. One of these sequences has very high homology to a sequence derived from the so-called MS-associated retrovirus (MSRV). Another cluster of three ERV sequences from the immunoglobulin heavy chain locus has retained the typical organization of retroviral genomes. These observations might shed new light on a possible association between ERVs and MS pathogenesis.

CNS innate immune cells sense pathogen/injury stimuli and co-ordinate inflammatory and tissue repair responses to protect and repair neurologic tissues. The major innate immune cells in the CNS were originally thought to be microglia, infiltrating monocytes and astrocytes but mast cells and innate lymphoid cells are now also known to play important roles. Disbalance in innate immune cells or their function may result in the lack of inflammation resolution, leading to chronic inflammatory maladaptive responses and disease. The study of innate immune cells in the CNS has revealed that innate immune cells regulate the recruitment of immune cells, adaptive immune responses and neuronal regeneration or death. These effects influence Multiple Sclerosis, spinal cord and brain injury recovery, as well as changes in stress and behavioral responses. Understanding how each cell contributes to molecular and cellular processes that impinge on neuroinflammation will be essential to devise strategies to diagnose or treat conditions such as CNS autoimmunity, traumatic brain injury, spinal cord injury, infections, Alzheimer’s disease and cancer among others. This Research Topic will provide a comprehensive overview of our current understanding of the mechanisms that modulate innate immune cell-driven CNS inflammatory/regulatory processes and their impact on CNS inflammatory disease pathogenesis, diagnosis and/or treatment. We seek articles that cover, but are not limited to, the followin

Discover the factors that inhibit axon regrowth following CNS injury and the potential therapeutics being developed to overome them

Mediators of Inflammation is a peer-reviewed, Open Access journal that publishes original research and review articles on all types of inflammatory mediators, including cytokines, histamine, bradykinin, prostaglandins, leukotrienes, PAF, biological response modifiers and the family of cell adhesion-promoting molecules.

European Commission

Parkinson’s disease (PD) and multiple system atrophy (MSA) are two neurodegenerative disorders and, so far, only treatment of the symptoms is available. European scientists have developed vaccines to reduce severity of the diseases and improve patient function.

Proliferation and activation of microglia in the brain, concentrated around amyloid plaques, is a prominent feature of Alzheimer’s disease (AD). Human genetics data point to a key role for microglia in the pathogenesis of AD. The majority of risk genes for AD are highly expressed (and many are selectively expressed) by microglia in the brain. There is mounting evidence that microglia protect against the incidence of AD, as impaired microglial activities and altered microglial responses to β-amyloid are associated with increased AD risk. On the other hand, there is also abundant evidence that activated microglia can be harmful to neurons. Microglia can mediate synapse loss by engulfment of synapses, likely via a complement-dependent mechanism; they can also exacerbate tau pathology and secrete inflammatory factors that can injure neurons directly or via activation of neurotoxic astrocytes. Gene expression profiles indicate multiple states of microglial activation in neurodegenerative disease settings, which might explain the disparate roles of microglia in the development and progression of AD pathology.

 The BRCA1 protein, one of the major players responsible for DNA damage response has recently been linked to Alzheimer’s disease (AD). Using primary fibroblasts and neurons reprogrammed from induced pluripotent stem cells (iPSC) derived from familial

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