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https://doi.org/10.3325/cmj.2013.54.419

Up-regulation of Synaptotagmin IV within amyloid plaqueassociated dystrophic neurons in Tg2576 mouse model of Alzheimer’s disease

Larisa Tratnjek ; Laboratory for Brain Research Institute of Pathophysiology, Medical Faculty University of Ljubljana, Ljubljana, Slovenia
Marko Živin ; Laboratory for Brain Research Institute of Pathophysiology, Medical Faculty University of Ljubljana, Ljubljana, Slovenia
Gordana Glavan ; Department of Biology, Biotehnical faculty, University of Ljubljana Ljubljana, Slovenia


Puni tekst: engleski pdf 2.813 Kb

str. 419-428

preuzimanja: 559

citiraj


Sažetak

Aim To investigate the involvement of the vesicular membrane
trafficking regulator Synaptotagmin IV (Syt IV) in
Alzheimer’s disease pathogenesis and to define the cell
types containing increased levels of Syt IV in the β-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 markers
for astrocytes (glial fibrillary acidic protein), microglia (major
histocompatibility complex class II), neurons (neuronal
specific nuclear protein), and neurites (neurofilaments)
were performed in WT and Tg2576 mouse cerebral cortex.
Results Western blot analysis showed higher Syt IV levels
in Tg2576 mice cortex than in WT cortex. Syt IV was found
only in neurons. In plaque vicinity, Syt IV was up-regulated
in dystrophic neurons. The Syt IV signal was not up-regulated
in the neurons of Tg2576 mice cortex without plaques
(resembling the pre-symptomatic conditions).
Conclusions Syt IV up-regulation within dystrophic neurons
probably reflects disrupted vesicular transport or/and
impaired protein degradation occurring in Alzheimer’s disease
and 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.

Ključne riječi

Hrčak ID:

113232

URI

https://hrcak.srce.hr/113232

Datum izdavanja:

15.10.2013.

Posjeta: 1.106 *