Alzheimer

Characteristic of Alzheimer´s disease is the accumulation of amyloid plaques in the brain. The major components of these plaques are 39-42 residue-long amyloid-β-peptides, which form insoluble fibrils via self-assembly. The amyloid-β-peptides are fragments of the broadly distributed, membrane-bound amyloid precursor protein APP, encoded on chromosome 21. They are formed from the proteolytic cleavage of APP by β- and γ-secretases.
Cleavage occurs after residue 40 or after residue 42. Even slightly increased amounts of amyloid-β-1-42 are described to be sufficient to cause Alzheimer's disease.
References:
M. Ahmed, J. Davis, D. Aucoin, T. Sato, S. Ahuja, S. Aimoto, J. I. Elliott, W. E. Van Nostrand, S. O. Smith (2010) Nat. Struct. Mol. Biol. 17, 561-567.
T. Hartmann, S. C. Bieger, B. Brühl, P. J. Tienari, N. Ida, D. Allsop, G. W. Roberts, C. L. Masters, C. G. Dotti, K. Unsicker, K. Beyreuther (1997) Nat. Med. 3, 1016-1020.

Characteristic of Alzheimer´s disease is the accumulation of amyloid plaques in the brain. The major components of these plaques are 39-42 residue-long amyloid-β-peptides, which form insoluble... read more »
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Alzheimer

Characteristic of Alzheimer´s disease is the accumulation of amyloid plaques in the brain. The major components of these plaques are 39-42 residue-long amyloid-β-peptides, which form insoluble fibrils via self-assembly. The amyloid-β-peptides are fragments of the broadly distributed, membrane-bound amyloid precursor protein APP, encoded on chromosome 21. They are formed from the proteolytic cleavage of APP by β- and γ-secretases.
Cleavage occurs after residue 40 or after residue 42. Even slightly increased amounts of amyloid-β-1-42 are described to be sufficient to cause Alzheimer's disease.
References:
M. Ahmed, J. Davis, D. Aucoin, T. Sato, S. Ahuja, S. Aimoto, J. I. Elliott, W. E. Van Nostrand, S. O. Smith (2010) Nat. Struct. Mol. Biol. 17, 561-567.
T. Hartmann, S. C. Bieger, B. Brühl, P. J. Tienari, N. Ida, D. Allsop, G. W. Roberts, C. L. Masters, C. G. Dotti, K. Unsicker, K. Beyreuther (1997) Nat. Med. 3, 1016-1020.

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[beta]-Amyloid (10-20) - YEVHHQKLVFF [beta]-Amyloid (10-20) - YEVHHQKLVFF
[beta]-Amyloid (10-20) (peptide sequence: YEVHHQKLVFF) ist used as a test peptide for the hydrophilic part of the complete Amyloid beta 1-42 peptide. Amyloid-beta (1-42) human is an Alzheimer desease peptide. Characteristic of Alzheimer...
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[beta]-Amyloid/A4 Protein Precursor (APP) (328 - 332) - RERMS [beta]-Amyloid/A4 Protein Precursor (APP) (328...
Amino acid sequence RERMS represents the active domain of amyloid beta/A4 protein precursor that promotes fibroblast growth; H. Ninomiya, et al.; J. Cell. Biol. 121, 879 (1993). The characteristic of Alzheimer disease is the accumulation...
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Ac-KLVFF-NH2 Ac-KLVFF-NH2
Ac-KLVFF-NH2 is the N-terminal and C-terminal modified form of the amyloid-beta (16-20) inhibitor peptid KLVFF. The modification leads to higher stability against peptidases. The KLVFF peptide is one of several inhibitors of amyloid-beta...
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Amyloid-beta (1-42), rat DAEFGHDSGFEVRHQKLVFFAEDVGSNKGAIIGLMVGGVVIA Amyloid-beta (1-42), rat...
[beta]-Amyloid (1-42), rat DAEFGHDSGFEVRHQKLVFFAEDVGSNKGAIIGLMVGGVVIA belongs to the Amyloid-ß-peptides. The characteristic of Alzheimer disease is the accumulation of amyloid plaques in the brain. The major components of these plaques...
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Amyloid-beta (16-20) KLVFF inhibitor peptide of Amyloid-beta Amyloid-beta (16-20) KLVFF inhibitor peptide of...
[beta]-Amyloid (16-20) - KLVFF (peptide sequence: KLVFF) ist used as a test peptide for the hydrophilic part of the complete Amyloid beta 1-40 peptide. The KLVFF peptide is one of several inhibitors of amyloid-beta aggregation that have...
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Amyloid-beta peptide PGRSPFTGKKLFNQEFSQDQ Amyloid-beta peptide PGRSPFTGKKLFNQEFSQDQ
Amyloid-beta peptide PGRSPFTGKKLFNQEFSQDQ. Several inhibitors of amyloid-beta aggregation have been published. Many of them are fragments and modified peptides derived from the native amyloid-beta sequence. Others were identified by...
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Control peptide Amyloid-beta (40-1) human Control peptide Amyloid-beta (40-1) human
Amyloid-ß-peptides: Characteristic of Alzheimer disease is the accumulation of amyloid plaques in the brain. The major components of these plaques are 39-42 residue-long amyloid-ß-peptides, which form insoluble fibrils via self-assembly....
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Control peptide Amyloid-beta (40-1) rat Control peptide Amyloid-beta (40-1) rat
Control peptide Amyloid-beta (40-1) rat. Characteristic of Alzheimer disease is the accumulation of amyloid plaques in the brain. The major components of these plaques are 39-42 residue-long amyloid-ß-peptides, which form insoluble...
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DWGKGGRWRLWPGASGKTEA - Inhibitor Peptide of amyloid-ß DWGKGGRWRLWPGASGKTEA - Inhibitor Peptide of...
The DWGKGGRWRLWPGASGKTEA peptide is one of several inhibitors of amyloid-beta aggregation that have been published. Many of them are fragments and modified peptides derived from the native amyloid-beta sequence. Others were identified by...
From €224.54 *
FYLKVPSSLHHHHGRDKLVFFHHHH FYLKVPSSLHHHHGRDKLVFFHHHH
Several inhibitors of amyloid-beta aggregation have been published. Many of them are fragments and modified peptides derived from the native amyloid-beta sequence. Others were identified by phage display approaches. An overview about...
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Alzheimer Peptide NYSKMIFSHHHH Peptide: NYSKMIFSHHHH
Several inhibitors of amyloid-beta aggregation have been published. Many of them are fragments and modified peptides derived from the native amyloid-beta sequence. Others were identified by phage display approaches. An overview about...
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RIIGL - Inhibitor Peptide of amyloid-ß RIIGL - Inhibitor Peptide of amyloid-ß
RIIGL is one of several inhibitors of amyloid-beta aggregation that have been published. Many of them are fragments and modified peptides derived from the native amyloid-beta sequence. Others were identified by phage display approaches....
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