Decreased levels of synaptosomal associated protein 25 in the brain of patients with Down Syndrome and Alzheimer's disease

Citation
S. Greber et al., Decreased levels of synaptosomal associated protein 25 in the brain of patients with Down Syndrome and Alzheimer's disease, ELECTROPHOR, 20(4-5), 1999, pp. 928-934
Citations number
38
Categorie Soggetti
Chemistry & Analysis
Journal title
ELECTROPHORESIS
ISSN journal
01730835 → ACNP
Volume
20
Issue
4-5
Year of publication
1999
Pages
928 - 934
Database
ISI
SICI code
0173-0835(199904/05)20:4-5<928:DLOSAP>2.0.ZU;2-0
Abstract
Synaptosomal associated protein 25 kDa (snap-25) is a widely distributed me mbrane-associated protein in the brain, mainly localized in nerve terminals . In nerve terminals, snap-25 participates in docking and/or fusion of syna ptic vesicles with the plasmalemma, a process essential for synaptic vesicl e exocytosis. Recent work suggests a role in brain development, forming pre synaptic sites by regulating axonal outgrowth and nerve growth-induced neur ite elongation. In Down syndrome (DS) brain, it is abnormally developed fro m early life, and brain pathology becomes even more pronounced when Alzheim er's disease (AD) develops in the fourth decade. This information led us to examine snap-25 in the brain of patients with DS and AD. We studied snap-2 5 and glial fibrillary acidic protein (GFAP) brain levels in five individua l brain areas of 9 aged patients with DS, 9 patients with AD and 9 controls , applying two-dimensional gel electrophoresis. Decreased snap-25 levels we re found in the five brain regions of the patients with DS and AD. Increase d expression levels of GFAP were found in the frontal, parietal, temporal a nd occipital cortex regions of the DS and AD patients. Decreased snap-25 pr otein levels in the brain of DS and AD may reflect impaired synaptogenesis or represent neuronal loss. Findings of increased GFAP, a marker for neuron al loss, along with data from literature would support the notion of decrea sed snap-25 secondary to neuronal decay in both neurodegenerative disorders .