149 research outputs found
Vascular consequences of passive Aβ immunization for Alzheimer's disease. Is avoidance of "malactivation" of microglia enough?
No full textAbstract The role of inflammation in Alzheimer's disease (AD) has been controversial since its first consideration. As with most instances of neuroinflammation, the possibility must be considered that activation of glia and cytokine networks in AD arises merely as a reaction to neurodegeneration. Active, healthy neurons produce signals that suppress inflammatory events, and dying neurons activate phagocytic responses in microglia at the very least. But simultaneous with the arrival of a more complex view of microglia, evidence that inflammation plays a causal or exacerbating role in AD etiology has been boosted by genetic, physiological, and epidemiological studies. In the end, it may be that the semantics of "inflammation" and glial "activation" must be regarded as too simplistic for the advancement of our understanding in this regard. It is clear that elaboration of the entire repertoire of activated microglia – a phenomenon that may be termed "malactivation" – must be prevented for healthy brain structure and function. Nevertheless, recent studies have suggested that phagocytosis of Aβ by microglia plays an important role in clearance of amyloid plaques, a process boosted by immunization paradigms. To the extent that this clearance might produce clinical improvements (still an open question), this relationship thus obligates a more nuanced consideration of the factors that indicate and control the various activities of microglia and other components of neuroinflammation.</p
Maternal obesity reprograms offspring's executive brain centers in a sex-specific manner?:An Editorial for "Perinatal high fat diet and early life methyl donor supplementation alter one carbon metabolism and DNA methylation in the brain" on page 362
No full textThis editorial highlights an article by McKee and colleagues in the current issue of Journal of Neurochemistry, in which the authors report epigenetic changes linked to one-carbon metabolism in prefrontal cortex (PFC) of murine offspring from dams fed high-fat diet to mimic maternal obesity. The group found that high-fat diet feeding in utero increases weight gain in offspring and dynamically alters DNA methylation in the PFC of male but not female brains. These epigenetic marks were associated with a shift in brain one-carbon metabolism (folate and methionine) intermediates and were normalized by early-life methyl-donor supplementation in a sex-specific manner.</p
Production and Functional Assays of Recombinant Secreted Amyloid Precursor Protein (APP) (sAPPα)
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