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Analysis of microdissected neurons by 18O mass spectrometry reveals altered protein expression in Alzheimer's disease.

Hashimoto M, Bogdanovic N, Nakagawa H, Volkmann I, Aoki M, Winblad B, Sakai J, Tjernberg LO - J. Cell. Mol. Med. (2012)

Bottom Line: These analyses confirmed the altered expression levels, and showed in many AD cases a pathological pattern.The expression levels found by this method showed poor correlation with the neuron-specific analysis.Hence, we conclude that cell-specific proteome analysis reveals differences in the proteome that cannot be detected by bulk analysis.

View Article: PubMed Central - PubMed

Affiliation: Karolinska Institutet and Dainippon Sumitomo Pharma Alzheimer Center, Department of Neurobiology, Care Sciences and Society, NVS, Karolinska Institutet, Huddinge, Sweden.

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S100B staining in the CA1 region. (A) Control, case number 6. (B, C) Sporadic AD cases, case numbers 9 and 8, respectively (Table 1). Magnification of originals: 40χ. Magnification of insets: 70χ. Scale bar corresponds to 50 μm.
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fig02: S100B staining in the CA1 region. (A) Control, case number 6. (B, C) Sporadic AD cases, case numbers 9 and 8, respectively (Table 1). Magnification of originals: 40χ. Magnification of insets: 70χ. Scale bar corresponds to 50 μm.

Mentions: In the control case, S100B was specifically expressed in astrocytes and oligodendrocytes (Fig. 2A). In AD cases, the immunoreactivity of S100B in astrocytes was increased as compared to the control case (Fig. 2A–C). S100B immunoreactivity was observed also in endothelial cells in capillaries. However, in one AD case, we detected immunoreactivity not only in glial cells but also in some pyramidal neurons (Fig. 2B, case number 9). We found another AD case to have a high intraneuronal expression of S100B (Fig. 2C, case number 8). In this case, some neurons lacked nuclear structure, suggesting that S100B could be involved in severe neurodegeneration and tangle formation.


Analysis of microdissected neurons by 18O mass spectrometry reveals altered protein expression in Alzheimer's disease.

Hashimoto M, Bogdanovic N, Nakagawa H, Volkmann I, Aoki M, Winblad B, Sakai J, Tjernberg LO - J. Cell. Mol. Med. (2012)

S100B staining in the CA1 region. (A) Control, case number 6. (B, C) Sporadic AD cases, case numbers 9 and 8, respectively (Table 1). Magnification of originals: 40χ. Magnification of insets: 70χ. Scale bar corresponds to 50 μm.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3822682&req=5

fig02: S100B staining in the CA1 region. (A) Control, case number 6. (B, C) Sporadic AD cases, case numbers 9 and 8, respectively (Table 1). Magnification of originals: 40χ. Magnification of insets: 70χ. Scale bar corresponds to 50 μm.
Mentions: In the control case, S100B was specifically expressed in astrocytes and oligodendrocytes (Fig. 2A). In AD cases, the immunoreactivity of S100B in astrocytes was increased as compared to the control case (Fig. 2A–C). S100B immunoreactivity was observed also in endothelial cells in capillaries. However, in one AD case, we detected immunoreactivity not only in glial cells but also in some pyramidal neurons (Fig. 2B, case number 9). We found another AD case to have a high intraneuronal expression of S100B (Fig. 2C, case number 8). In this case, some neurons lacked nuclear structure, suggesting that S100B could be involved in severe neurodegeneration and tangle formation.

Bottom Line: These analyses confirmed the altered expression levels, and showed in many AD cases a pathological pattern.The expression levels found by this method showed poor correlation with the neuron-specific analysis.Hence, we conclude that cell-specific proteome analysis reveals differences in the proteome that cannot be detected by bulk analysis.

View Article: PubMed Central - PubMed

Affiliation: Karolinska Institutet and Dainippon Sumitomo Pharma Alzheimer Center, Department of Neurobiology, Care Sciences and Society, NVS, Karolinska Institutet, Huddinge, Sweden.

Show MeSH
Related in: MedlinePlus