Aim To investigate the involvement of the vesicular membrane trafficking regulator Synaptotagmin IV (Syt IV) in Alzheimers disease pathogenesis and to define the cell types containing increased ...levels of Syt IV in the -amyloid plaque vicinity. Methods Syt IV protein levels in wild type (WT) and Tg2576 mice cortex were determined by Western blot analysis and immunohistochemistry. Co-localization studies using double immunofluorescence staining for Syt IV and markersfor astrocytes (glial fibrillary acidic protein), microglia (major histocompatibility complex class II), neurons (neuronalspecific nuclear protein), and neurites (neurofilaments) were performed in WT and Tg2576 mouse cerebral cortex. Results Western blot analysis showed higher Syt IV levelsin Tg2576 mice cortex than in WT cortex. Syt IV was foundonly in neurons. In plaque vicinity, Syt IV was up-regulatedin dystrophic neurons. The Syt IV signal was not up-regulatedin the neurons of Tg2576 mice cortex without plaques (resembling the pre-symptomatic conditions). Conclusions Syt IV up-regulation within dystrophic neuronsprobably reflects disrupted vesicular transport or/and impaired protein degradation occurring in Alzheimers diseaseand is probably a consequence but not the cause of neuronal degeneration. Hence, Syt IV up-regulation and/or its accumulation in dystrophic neurons may have adverse effects on the survival of the affected neuron.
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