Serrano-Pozo A, Frosch MP, Masliah E, Hyman BT. Neuropathological alterations in Alzheimer disease. Cold Spring Harb Perspect Med. 2011;1:a006189.
Article
PubMed
PubMed Central
Google Scholar
Hardy J, Allsop D. Amyloid deposition as the central event in the aetiology of Alzheimer’s disease. Trends Pharmacol Sci. 1991;12:383–8.
Article
CAS
PubMed
Google Scholar
O’Brien RJ, Wong PC. Amyloid precursor protein processing and Alzheimer’s disease. Annu Rev Neurosci. 2011;34:185–204.
Article
PubMed
PubMed Central
Google Scholar
Beher D, Wrigley JD, Owens AP, Shearman MS. Generation of C-terminally truncated amyloid-β peptides is dependent on γ-secretase activity. J Neurochem. 2002;82:563–75.
Article
CAS
PubMed
Google Scholar
Reinert J, Richard BC, Klafki HW, Friedrich B, Bayer TA, Wiltfang J, Kovacs GG, Ingelsson M, Lannfelt L, Paetau A, et al. Deposition of C-terminally truncated Aβ species Aβ37 and Aβ39 in Alzheimer’s disease and transgenic mouse models. Acta Neuropathol Commun. 2016;4:24.
Article
PubMed
PubMed Central
Google Scholar
Saito T, Suemoto T, Brouwers N, Sleegers K, Funamoto S, Mihira N, Matsuba Y, Yamada K, Nilsson P, Takano J, et al. Potent amyloidogenicity and pathogenicity of Aβ43. Nat Neurosci. 2011;14:1023–32.
Article
CAS
PubMed
Google Scholar
Savastano A, Klafki H, Haussmann U, Oberstein TJ, Muller P, Wirths O, Wiltfang J, Bayer TA. N-truncated Aβ2–X starting with position two in sporadic Alzheimer’s disease cases and two Alzheimer mouse models. J Alzheimers Dis. 2016;49:101–10.
Article
PubMed
Google Scholar
Wirths O, Bethge T, Marcello A, Harmeier A, Jawhar S, Lucassen PJ, Multhaup G, Brody DL, Esparza T, Ingelsson M, et al. Pyroglutamate Aβ pathology in APP/PS1KI mice, sporadic and familial Alzheimer’s disease cases. J Neural Transm. 2010;117:85–96.
Article
CAS
PubMed
Google Scholar
Iwatsubo T, Saido TC, Mann DM, Lee VM, Trojanowski JQ. Full-length amyloid-β(1–42(43)) and amino-terminally modified and truncated amyloid-β42(43) deposit in diffuse plaques. Am J Pathol. 1996;149:1823–30.
CAS
PubMed
PubMed Central
Google Scholar
Guzman EA, Bouter Y, Richard BC, Lannfelt L, Ingelsson M, Paetau A, Verkkoniemi-Ahola A, Wirths O, Bayer TA. Abundance of Aβ5–xlike immunoreactivity in transgenic 5XFAD, APP/PS1KI and 3xTG mice, sporadic and familial Alzheimer’s disease. Mol Neurodegener. 2014;9:13.
Article
PubMed
PubMed Central
Google Scholar
Takeda K, Araki W, Akiyama H, Tabira T. Amino-truncated amyloid β-peptide (Aβ5-40/42) produced from caspase-cleaved amyloid precursor protein is deposited in Alzheimer’s disease brain. FASEB J. 2004;18:1755–7.
CAS
PubMed
Google Scholar
Liu K, Solano I, Mann D, Lemere C, Mercken M, Trojanowski JQ, Lee VM. Characterization of Aβ11-40/42 peptide deposition in Alzheimer’s disease and young Down’s syndrome brains: implication of N-terminally truncated Aβ species in the pathogenesis of Alzheimer’s disease. Acta Neuropathol (Berl). 2006;112:163–74.
Article
CAS
Google Scholar
Sullivan CP, Berg EA, Elliott-Bryant R, Fishman JB, McKee AC, Morin PJ, Shia M, Fine RE. Pyroglutamate-Aβ 3 and 11 colocalize in amyloid plaques in Alzheimer’s disease cerebral cortex with pyroglutamate-Aβ 11 forming the central core. Neurosci Lett. 2011;505:109–12.
Article
CAS
PubMed
PubMed Central
Google Scholar
Portelius E, Bogdanovic N, Gustavsson MK, Volkmann I, Brinkmalm G, Zetterberg H, Winblad B, Blennow K. Mass spectrometric characterization of brain amyloid β isoform signatures in familial and sporadic Alzheimer’s disease. Acta Neuropathol. 2010;120:185–93.
Article
CAS
PubMed
PubMed Central
Google Scholar
Moore BD, Chakrabarty P, Levites Y, Kukar TL, Baine AM, Moroni T, Ladd TB, Das P, Dickson DW, Golde TE. Overlapping profiles of Aβ peptides in the Alzheimer’s disease and pathological aging brains. Alzheimers Res Ther. 2012;4:18.
Article
CAS
PubMed
PubMed Central
Google Scholar
Kummer MP, Heneka MT. Truncated and modified amyloid-β species. Alzheimers Res Ther. 2014;6:28.
Article
PubMed
PubMed Central
Google Scholar
Bayer TA, Wirths O. Focusing the amyloid cascade hypothesis on N-truncated Aβ peptides as drug targets against Alzheimer’s disease. Acta Neuropathol. 2014;127:787–801.
Article
CAS
PubMed
PubMed Central
Google Scholar
Pike CJ, Overman MJ, Cotman CW. Amino-terminal deletions enhance aggregation of β-amyloid peptides in vitro. J Biol Chem. 1995;270:23895–8.
Article
CAS
PubMed
Google Scholar
Masters CL, Simms G, Weinman NA, Multhaup G, McDonald BL, Beyreuther K. Amyloid plaque core protein in Alzheimer disease and Down syndrome. Proc Natl Acad Sci U S A. 1985;82:4245–9.
Article
CAS
PubMed
PubMed Central
Google Scholar
Miller DL, Papayannopoulos IA, Styles J, Bobin SA, Lin YY, Biemann K, Iqbal K. Peptide compositions of the cerebrovascular and senile plaque core amyloid deposits of Alzheimer’s disease. Arch Biochem Biophys. 1993;301:41–52.
Article
CAS
PubMed
Google Scholar
Portelius E, Lashley T, Westerlund A, Persson R, Fox NC, Blennow K, Revesz T, Zetterberg H. Brain amyloid-β fragment signatures in pathological ageing and Alzheimer’s disease by hybrid immunoprecipitation mass spectrometry. Neurodegener Dis. 2015;15:50–7.
Article
CAS
PubMed
Google Scholar
Oberstein TJ, Spitzer P, Klafki H-W, Linning P, Neff F, Knölker HJ, Lewczuk P, Wiltfang J, Kornhuber J, Maler JM. Astrocytes and microglia but not neurons preferentially generate N-terminally truncated Aβ peptides. Neurobiol Dis. 2015;73:24–35.
Article
CAS
PubMed
Google Scholar
Haussmann U, Jahn O, Linning P, Janssen C, Liepold T, Portelius E, Zetterberg H, Bauer C, Schuchhardt J, Knolker HJ, et al. Analysis of amino-terminal variants of amyloid-β peptides by capillary isoelectric focusing immunoassay. Anal Chem. 2013;85:8142–9.
Article
CAS
PubMed
Google Scholar
Wiltfang J, Esselmann H, Cupers P, Neumann M, Kretzschmar H, Beyermann M, Schleuder D, Jahn H, Ruther E, Kornhuber J, et al. Elevation of β-amyloid peptide 2-42 in sporadic and familial Alzheimer’s disease and its generation in PS1 knockout cells. J Biol Chem. 2001;276:42645–57.
Article
CAS
PubMed
Google Scholar
Hahn S, Bruning T, Ness J, Czirr E, Baches S, Gijsen H, Korth C, Pietrzik CU, Bulic B, Weggen S. Presenilin-1 but not amyloid precursor protein mutations present in mouse models of Alzheimer’s disease attenuate the response of cultured cells to γ-secretase modulators regardless of their potency and structure. J Neurochem. 2011;116:385–95.
Article
CAS
PubMed
Google Scholar
Casas C, Sergeant N, Itier JM, Blanchard V, Wirths O, van der Kolk N, Vingtdeux V, van de Steeg E, Ret G, Canton T, et al. Massive CA1/2 neuronal loss with intraneuronal and N-terminal truncated Aβ 42 accumulation in a novel Alzheimer transgenic model. Am J Pathol. 2004;165:1289–300.
Article
CAS
PubMed
PubMed Central
Google Scholar
Jawhar S, Trawicka A, Jenneckens C, Bayer TA, Wirths O. Motor deficits, neuron loss, and reduced anxiety coinciding with axonal degeneration and intraneuronal Aβ aggregation in the 5XFAD mouse model of Alzheimer’s disease. Neurobiol Aging. 2012;33:196. e129–40.
Article
PubMed
Google Scholar
Richard BC, Kurdakova A, Baches S, Bayer TA, Weggen S, Wirths O. Gene dosage dependent aggravation of the neurological phenotype in the 5XFAD mouse model of Alzheimer’s disease. J Alzheimers Dis. 2015;45:1223–36.
CAS
PubMed
Google Scholar
Brockhaus M, Grunberg J, Rohrig S, Loetscher H, Wittenburg N, Baumeister R, Jacobsen H, Haass C. Caspase-mediated cleavage is not required for the activity of presenilins in amyloidogenesis and NOTCH signaling. Neuroreport. 1998;9:1481–6.
Article
CAS
PubMed
Google Scholar
Antonios G, Saiepour N, Bouter Y, Richard B, Paetau A, Verkkoniemi-Ahola A, Lannfelt L, Ingelsson M, Kovacs G, Pillot T, et al. N-truncated Aβ starting with position four: early intraneuronal accumulation and rescue of toxicity using NT4X-167, a novel monoclonal antibody. Acta Neuropathol Commun. 2013;1:56.
Article
PubMed
PubMed Central
Google Scholar
Sergeant N, Bombois S, Ghestem A, Drobecq H, Kostanjevecki V, Missiaen C, Wattez A, David JP, Vanmechelen E, Sergheraert C, Delacourte A. Truncated β-amyloid peptide species in pre-clinical Alzheimer’s disease as new targets for the vaccination approach. J Neurochem. 2003;85:1581–91.
Article
CAS
PubMed
Google Scholar
Wirths O, Multhaup G, Czech C, Blanchard V, Moussaoui S, Tremp G, Pradier L, Beyreuther K, Bayer TA. Intraneuronal Aβ accumulation precedes plaque formation in β-amyloid precursor protein and presenilin-1 double-transgenic mice. Neurosci Lett. 2001;306:116–20.
Article
CAS
PubMed
Google Scholar
Bouter Y, Dietrich K, Wittnam JL, Rezaei-Ghaleh N, Pillot T, Papot-Couturier S, Lefebvre T, Sprenger F, Wirths O, Zweckstetter M, Bayer TA. N-truncated amyloid β (Aβ) 4-42 forms stable aggregates and induces acute and long-lasting behavioral deficits. Acta Neuropathol. 2013;126:189–205.
Article
CAS
PubMed
PubMed Central
Google Scholar
Lewis H, Beher D, Cookson N, Oakley A, Piggott M, Morris CM, Jaros E, Perry R, Ince P, Kenny RA, et al. Quantification of Alzheimer pathology in ageing and dementia: age-related accumulation of amyloid-β(42) peptide in vascular dementia. Neuropathol Appl Neurobiol. 2006;32:103–18.
Article
CAS
PubMed
Google Scholar
Kuo YM, Kokjohn TA, Beach TG, Sue LI, Brune D, Lopez JC, Kalback WM, Abramowski D, Sturchler-Pierrat C, Staufenbiel M, Roher AE. Comparative analysis of amyloid-β chemical structure and amyloid plaque morphology of transgenic mouse and Alzheimer’s disease brains. J Biol Chem. 2001;276:12991–8.
Article
CAS
PubMed
Google Scholar
Kalback W, Watson MD, Kokjohn TA, Kuo YM, Weiss N, Luehrs DC, Lopez J, Brune D, Sisodia SS, Staufenbiel M, et al. APP transgenic mice Tg2576 accumulate Aβ peptides that are distinct from the chemically modified and insoluble peptides deposited in Alzheimer’s disease senile plaques. Biochemistry. 2002;41:922–8.
Article
CAS
PubMed
Google Scholar
Sevalle J, Amoyel A, Robert P, Fournie-Zaluski MC, Roques B, Checler F. Aminopeptidase A contributes to the N-terminal truncation of amyloid β-peptide. J Neurochem. 2009;109:248–56.
Article
CAS
PubMed
Google Scholar
Bien J, Jefferson T, Čaušević M, Jumpertz T, Munter L, Multhaup G, Weggen S, Becker-Pauly C, Pietrzik CU. The metalloprotease meprin β generates amino terminal-truncated amyloid β peptide species. J Biol Chem. 2012;287:33304–13.
Article
CAS
PubMed
PubMed Central
Google Scholar
Lyons B, Friedrich MG, Raftery MJ, Truscott RJW. Amyloid plaque in the human brain can decompose from Aβ1-40/1-42 by spontaneous non-enzymatic processes. Anal Chem. 2016;88(5):2675–84.
Article
CAS
PubMed
Google Scholar
Rudinskiy N, Fuerer C, Demurtas D, Zamorano S, De Piano C, Herrmann AG, Spires-Jones TL, Oeckl P, Otto M, Frosch MP, et al. Amyloid-β oligomerization is associated with the generation of a typical peptide fragment fingerprint. Alzheimers Dement. 2016;12:996–1013.
Article
PubMed
Google Scholar