Dilaton-Axion hair for slowly rotating Kerr black holes

Campbell et al. demonstrated the existence of axion ``hair'' for Kerr black holes due to the non-trivial Lorentz Chern-Simons term and calculated it explicitly for the case of slow rotation. Here we consider the dilaton coupling to the axion field strength, consistent with low energy string theory and calculate the dilaton ``hair'' arising from this specific axion source.Comment: 13 pages + 1 fi

The growth-associated protein B-50 (GAP-43) in dystrophic neurites extending into Alzheimer's plaques

The expression of the growth associated protein B-50 (GAP-43) is developmentally regulated and reinduced following neuronal injury. Using B-50 as marker for sprouting in single and double immunolabeling of neocortex of Alzheimer's disease (AD) we demonstrate that bulbous B-50 immunoreactive dystrophic neurites are found in β-amyloid/A4 positive plaques. Our results and those of others indicate that dystrophic neurites contain B-50 implicating this protein in the disease induced response

Laser microdissection for spatial proteomics of postmortem brain tissue

Quantitative data of the proteome is highly valuable for providing unbiased information on protein expression changes related to disease or identifying related biomarkers. In brain diseases the affected area can be small and pathogenic events can be related to a specific cell type in an otherwise heterogeneous tissue type. An emerging approach dedicated to analysing this type of samples is laser microdissection (LMD) combined with LC-MS/MS into a single workflow. In this chapter, we describe two LMD methods for isolating tissue at the level of a small area and individual cells suitable for subsequent LC-MS/MS analysis

The neuroinflammatory response in plaques and amyloid angiopathy in Alzheimer's disease: Therapeutic implications

The amyloid plaques in Alzheimer's disease (AD) brains are co-localised with a broad variety of inflammation-related proteins (complement proteins, acute-phase proteins, pro-inflammatory cytokines) and clusters of activated microglia. The present data suggest that the Aβ depositions in the neuroparenchyma are closely associated with a locally-induced, non-immune-mediated chronic inflammatory response. Clinicopathological and neuroradiological data show that activation of microglia are a relatively early pathogenic event that precedes the process of severe neuropil destruction in patients. Recent gene findings (cDNA microarray) confirm the immunohistochemical findings of an early involvement of inflammatory and regenerative pathways in AD pathogenesis. Aβ deposition, inflammation and regenerative mechanisms are also early pathogenic events in transgenic mice models harbouring the pathological AD mutations, while "later" neurodegenerative characteristics are not seen in these models. Next to the plaques, Aβ amyloid deposition is frequently found in the walls of cerebral vessels (cerebral amyloid angiopathy). Most common is the type of amyloid deposition in the walls of meningeal and medium-sized cortical arteries, and more rarely, microcapillary amyloid angiopathy (dyshoric angiopathy). Immunohistochemical studies show that in AD patients, the majority of the amyloid deposits in the walls of the larger vessels is not associated with a chronic inflammatory response in contrast to micro-capillary amyloid angiopathy. In this contribution, we will give an overview of the similarities and differences between the involvement of inflammatory mechanisms in vascular and plaque amyloid in AD and transgenic models. The implications of the reviewed studies for an inflammation-based therapeutical approach in AD will be discussed

Microglia, amyloid and dementia in Alzheimer disease. A correlative study.

To elucidate the role of microglia in Alzheimer's disease, a clinicopathological study was performed involving 26 cases, the mental status of which had been studied pre mortem by the Blessed test score (BTS). We measured the volume density of CD 68 immunoreactive (IR) microglia, congophilic plaques and Abeta deposits, and the numerical density of neurofibrillary tangles (NFT) in a sample of Area 9 (middle frontal gyrus). Dementia was significantly correlated only with the volume density of Abeta deposits and the numerical density of NFT. The volume densities of microglia and congophilic plaques were strongly correlated. With the intellectual status used as a time scale, IR microglia and amyloid deposits appeared almost simultaneously at an early stage in the pathological cascade and decreased, whereas Abeta and NFT were still accumulating. The intellectual deficit seemed to be more significantly related to the latter two lesions than to the microglia-amyloid complex, that was visible at an earlier stage (around BTS = 15

Panencephalopathic Creutzfeldt-Jakob disease in the Netherlands and the UK: Clinical and pathological characteristics of nine patients

Aims: The panencephalopathic type of Creutzfeldt-Jakob disease (PECJD) has extensive abnormalities in cerebral white matter as well as the cortex. PECJD has rarely been described in Caucasians and debate continues on its classification and pathogenesis. We describe our experience of PECJD over a 14-year period of surveillance for CJD in the Netherlands and the UK. Methods: Between 1993 and 2006, nine cases of PECJD were identified. Clinical, histological and biochemical characteristics of all patients were analysed and compared; all cases were classified clinically as sporadic CJD. Results: The median age at onset was 57.8 years and median disease duration was 22 months. The average brain weight was 887 g. Most patients showed a two-stage clinical course with initial rapid deterioration to a state of akinetic mutism, which then persisted over a longer time scale. Neuropathological findings were characterized by severe global atrophy with status spongiosus. Cerebral white matter involvement tended to be associated with either disease duration or severity of cerebral cortical lesions. Five patients could be classified into the MM1 subtype of sporadic CJD, one patient into the MM2 subgroup and another into the MV2 subgroup. Two patients were heterozygous at codon 129 in the prion protein gene and contained both type 1 and type 2 PrPres isoforms in the brain. Conclusions: We believe that white matter pathology in PECJD represents an end-stage pattern that reflects secondary degeneration due to widespread cortical neuronal loss that occurs in the early part of the disease, rather than representing a primary lesion

A laser microdissection–liquid chromatography–tandem mass spectrometry workflow for post-mortem analysis of brain tissue

Improved speed and sensitivity of mass spectrometry allow the simultaneous quantification of high numbers of proteins from increasingly smaller quantities of tissue sample. Quantitative data of the proteome is highly valuable for providing unbiased information on, for example, protein expression changes related to disease or identifying related biomarkers. In brain diseases the affected area can be small and pathogenic events can be related to a specific cell type in an otherwise heterogeneous tissue type. An emerging approach dedicated to analyzing this type of samples is laser micro-dissection (LMD) combined with LC-MS/MS into a single workflow. In this chapter, we describe different options for isolating tissue suitable for LC-MS/MS analysis

Laser microdissection for spatial proteomics of postmortem brain tissue

Quantitative data of the proteome is highly valuable for providing unbiased information on protein expression changes related to disease or identifying related biomarkers. In brain diseases the affected area can be small and pathogenic events can be related to a specific cell type in an otherwise heterogeneous tissue type. An emerging approach dedicated to analysing this type of samples is laser microdissection (LMD) combined with LC-MS/MS into a single workflow. In this chapter, we describe two LMD methods for isolating tissue at the level of a small area and individual cells suitable for subsequent LC-MS/MS analysis