Formic acid is essential for immunohistochemical detection of aggregated intraneuronal Aβ peptides in mouse models of Alzheimer's disease

被引:28
作者
Christensen, Ditte Z.
Bayer, Thomas A.
Wirths, Oliver [1 ]
机构
[1] Univ Gottingen, Div Mol Psychiat, D-37075 Gottingen, Germany
关键词
Intracellular Abeta; Intraneuronal Abeta; Aggregated Abeta; Alzheimer; Staining; Transgenic mice; Amyloid; Formic acid; Heat; AMYLOID PRECURSOR PROTEIN; PLAQUE-FORMATION; TRANSGENIC MICE; A-BETA-42; ACCUMULATION; PYRAMIDAL NEURONS; DOWN-SYNDROME; PRESENILIN-1; BRAIN; NEURODEGENERATION; MUTATIONS;
D O I
10.1016/j.brainres.2009.09.014
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The staining protocols so far applied to study intracellular A beta accumulation in human tissue have been inconsistent with varying use of heat and formic acid (FA) for antigen retrieval. Microwave heat treatment has been reported to enhance the staining of intraneuronal A beta as compared to no or enzymatic pretreatment. FA is widely used to increase the staining of plaque pathology in AD, yet the effect of FA on intraneuronal A staining has been reported to be low and similar to the effect of heat or even to counteract the enhancing effect of heat pretreatment on intraneuronal A beta immunohistochemical detection. To overcome these inconsistencies, there is a need for optimization of the staining protocol for intraneuronal. A beta detection and more knowledge is required concerning the effects of the different antigen retrieval methods. in the present work, we optimized the staining protocol for intraneuronal A beta in paraffin-embedded sections in relation to heat and FA using four different mouse models known to accumulate intraneuronal A beta peptides. It was found that FA is essential for the staining of highly aggregated intraneuronal A beta peptides in AD transgenic mouse tissue. (C) 2009 Elsevier B.V. All rights reserved
引用
收藏
页码:116 / 125
页数:10
相关论文
共 48 条
[1]   Frequent Amyloid Deposition Without Significant Cognitive Impairment Among the Elderly [J].
Aizenstein, Howard Jay ;
Nebes, Robert D. ;
Saxton, Judith A. ;
Price, Julie C. ;
Mathis, Chester A. ;
Tsopelas, Nicholas D. ;
Ziolko, Scott K. ;
James, Jeffrey A. ;
Snitz, Beth E. ;
Houck, Patricia R. ;
Bi, Wenzhu ;
Cohen, Ann D. ;
Lopresti, Brian J. ;
DeKosky, Steven T. ;
Halligan, Edythe M. ;
Klunk, William E. .
ARCHIVES OF NEUROLOGY, 2008, 65 (11) :1509-1517
[2]   Inter-laboratory comparison of neuropathological assessments of β-amyloid protein:: a study of the BrainNet Europe consortium [J].
Alafuzoff, Irina ;
Pikkarainen, Maria ;
Arzberger, Thomas ;
Thal, Dietmar R. ;
Al-Sarraj, Safa ;
Bell, Jeanne ;
Bodi, Istvan ;
Budka, Herbert ;
Capetillo-Zarate, Estibaliz ;
Ferrer, Isidro ;
Gelpi, Ellen ;
Gentleman, Stephen ;
Giaccone, Giorgio ;
Kavantzas, Nikolaos ;
King, Andrew ;
Korkolopoulou, Penelope ;
Kovacs, Gabor G. ;
Meyronet, David ;
Monoranu, Camelia ;
Parchi, Piero ;
Patsouris, Efstratios ;
Roggendorf, Wolfgang ;
Stadelmann, Christine ;
Streichenberger, Nathalie ;
Tagliavini, Fabricio ;
Kretzschmar, Hans .
ACTA NEUROPATHOLOGICA, 2008, 115 (05) :533-546
[3]   β-amyloid accumulation impairs multivesicular body sorting by inhibiting the ubiquitin-proteasome system [J].
Almeida, CG ;
Takahashi, RH ;
Gouras, GK .
JOURNAL OF NEUROSCIENCE, 2006, 26 (16) :4277-4288
[4]   Beta-amyloid accumulation in APP mutant neurons reduces PSD-95 and GluR1 in synapses [J].
Almeida, CG ;
Tampellini, D ;
Takahashi, RH ;
Greengard, P ;
Lin, MT ;
Snyder, EM ;
Gouras, GK .
NEUROBIOLOGY OF DISEASE, 2005, 20 (02) :187-198
[5]   Amyloid β-peptide levels in laser capture microdissected cornu ammonis I pyramidal neurons of Alzheimer's brain [J].
Aoki, Mikio ;
Volkmann, Inga ;
Tjernberg, Lars O. ;
Winblad, Bengt ;
Bogdanovic, Nenad .
NEUROREPORT, 2008, 19 (11) :1085-1089
[6]   APP/PS1KI bigenic mice develop early synaptic deficits and hippocampus atrophy [J].
Breyhan, Henning ;
Wirths, Oliver ;
Duan, Kailai ;
Marcello, Andrea ;
Rettig, Jens ;
Bayer, Thomas A. .
ACTA NEUROPATHOLOGICA, 2009, 117 (06) :677-685
[7]   Massive CA1/2 neuronal loss with intraneuronal and N-interminal truncated Aβ42 accumulation in a novel Alzheimer transgenic model [J].
Casas, C ;
Sergeant, N ;
Itier, JM ;
Blanchard, V ;
Wirths, O ;
van der Kolk, N ;
Vingtdeux, V ;
van de Steeg, E ;
Ret, G ;
Canton, T ;
Drobecq, H ;
Clark, A ;
Bonici, B ;
Delacourte, A ;
Benavides, J ;
Schmitz, C ;
Tremp, G ;
Bayer, TA ;
Benoit, P ;
Pradier, L .
AMERICAN JOURNAL OF PATHOLOGY, 2004, 165 (04) :1289-1300
[8]   Transient intraneuronal Aβ rather than extracellular plaque pathology correlates with neuron loss in the frontal cortex of APP/PS1KI mice [J].
Christensen, Ditte Zerlang ;
Kraus, Sophie Luise ;
Flohr, Antonius ;
Cotel, Marie-Caroline ;
Wirths, Oliver ;
Bayer, Thomas A. .
ACTA NEUROPATHOLOGICA, 2008, 116 (06) :647-655
[9]  
CHRISTENSEN DZ, 2008, NEUROBIOL AGING, V4, pT213
[10]   Transgenic mice with Alzheimer presenilin 1 mutations show accelerated neurodegeneration without amyloid plaque formation [J].
Chui, DH ;
Tanahashi, H ;
Ozawa, K ;
Ikeda, S ;
Checler, F ;
Ueda, O ;
Suzuki, H ;
Araki, W ;
Inoue, H ;
Shirotani, K ;
Takahashi, K ;
Gallyas, F ;
Tabira, T .
NATURE MEDICINE, 1999, 5 (05) :560-564