Harald Neumann

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The genetics of complex disease produce alterations in the molecular interactions of cellular pathways whose collective effect may become clear through the organized structure of molecular networks. To characterize molecular systems associated with late-onset Alzheimer's disease (LOAD), we constructed gene-regulatory networks in 1,647 postmortem brain(More)
Elimination of apoptotic neurons without inflammation is crucial for brain tissue homeostasis, but the molecular mechanism has not been firmly established. Triggering receptor expressed on myeloid cells-2 (TREM2) is a recently identified innate immune receptor. Here, we show expression of TREM2 in microglia. TREM2 stimulation induced DAP12 phosphorylation,(More)
Recent findings indicate that neurons are not merely passive targets of microglia but rather control microglial activity. The variety of different signals that neurons use to control microglia can be divided into two categories: 'Off' signals constitutively keep microglia in their resting state and antagonize proinflammatory activity. 'On' signals are(More)
Microglia are cells of myeloid origin that populate the CNS during early development and form the brain's innate immune cell type. They perform homoeostatic activity in the normal CNS, a function associated with high motility of their ramified processes and their constant phagocytic clearance of cell debris. This debris clearance role is amplified in CNS(More)
The immune status of the central nervous system (CNS) is strictly regulated. In the healthy brain, immune responses are kept to a minimum. In contrast, in a variety of inflammatory and neurodegenerative diseases, including multiple sclerosis, infections, trauma, stroke, neoplasia, and Alzheimer's disease, glial cells such as microglia gain(More)
Although the CNS is an established immune-privileged site, it is under surveillance by the immune system, particularly under pathological conditions. In the current study we examined the lymphocyte infiltration, a key component of this neuroimmune surveillance, into the axotomized facial motor nucleus and analyzed the changes in proinflammatory cytokines(More)
Cytotoxic T lymphocytes (CTLs) with a CD8(+) phenotype have the potential to recognize and attack major histocompatibility complex (MHC) class I-expressing brain cells. Most brain cells, including neurons, can be stimulated to present peptides to CD8(+) CTLs by MHC class I molecules, and are susceptible to CTL-mediated cytotoxicity in culture. In(More)
Microglial cells are of hematopoietic origin, populate the CNS during early development and form the brain's innate immune cell type. Besides their well-known role in immune defense, microglia have an active and homeostatic function in the normal CNS based on high motility of their ramified processes and endocytic clearance of apoptotic vesicular material.(More)
Damage to neurites with transection of axons and spheroid formation is commonly noted in the central nervous system during viral and autoimmune diseases such as multiple sclerosis, but it remains open whether such changes are caused primarily by immune mechanisms or whether they are secondary to inflammation. The present experiments explored whether(More)
NF-kappa B is inducible transcription factor present in many cell types in a latent cytoplasmic form. So far, only immune cells including mature B cells, thymocytes, and adherent macrophages have been reported to contain constitutively active forms of NF-kappa B in the nucleus. A recent study showed that the human immunodeficiency virus type 1 (HIV-1)(More)