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Key Documents

SCP0038

Sigma-Aldrich

Amyloid β 1-42 rat

≥90% (HPLC)

Synonym(s):

β-Amyloid 1-42, Amyloid for Rat, Rat Amyloid β 1-42

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About This Item

Empirical Formula (Hill Notation):
C199H307N53O59S1
Molecular Weight:
4417.95
UNSPSC Code:
12352200
NACRES:
NA.32

Assay

≥90% (HPLC)

form

lyophilized

composition

Peptide Content, ≥75%

storage condition

protect from light

storage temp.

−20°C

Amino Acid Sequence

Asp-Ala-Glu-Phe-Gly-His-Asp-Ser-Gly-Phe-Glu-Val-Arg-His-Gln-Lys-Leu-Val-Phe-Phe-Ala-Glu-Asp-Val-Gly-Ser-Asn-Lys-Gly-Ala-Ile-Ile-Gly-Leu-Met-Val-Gly-Gly-Val-Val-Ile-Ala

General description

Amyloid β (Aβ) 1-42 is the major Aβ species in the amyloid plaques that develop in the case of Alzheimer′s disease (AD). It has a cross-β structure with parallel, in-register β-sheets.

Application

Amyloid β 1-42 rat has been used as an amyloid β (Aβ) oligomer in intracerebroventricular (ICV) injection/intra-hippocampal infusion to establish the Alzheimer′s disease (AD) model in rat.

Biochem/physiol Actions

Amyloid β 1-42 forms amyloid fibrils more readily compared to Aβ(1–40), in vitro. Aβ1-42 injections are known to cause brain dysfunction indicating learning and memory deficits. Amyloid β (Aβ) refers to peptides derived from amyloid precursor protein that vary in length from 37–43 amino acids. Aβ(s) peptides, their peptide fragments, and mutated fragments are used to study a wide range of metabolic and regulatory functions including activation of kinases, regulation of cholesterol transport, function as a transcription factor, and regulators of inflammation. Aβ(s) peptides and their peptide fragments are also used to study oxidative stress, metal binding, and mechanisms of protein cross-linking in the context of diseases such as Alzheimer′s disease and neurodegeneration.

Storage Class Code

11 - Combustible Solids

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


Certificates of Analysis (COA)

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Volodymyr A Yavorsky et al.
Frontiers in cellular neuroscience, 17, 1132092-1132092 (2023-05-01)
One of the signs of Alzheimer's disease (AD) is the formation of β-amyloid plaques, which ultimately lead to the dysfunction of neurons with subsequent neurodegeneration. Although extensive researches have been conducted on the effects of different amyloid conformations such as
Enes Akyuz et al.
Biomedicines, 8(3) (2020-03-19)
Alzheimer's disease (AD) is a progressive neurodegenerative disorder with a complex etiology and characterized by cognitive deficits and memory loss. The pathogenesis of AD is not yet completely elucidated, and no curative treatment is currently available. Inwardly rectifying potassium (Kir)
Raheleh Farahzadi et al.
ACS chemical neuroscience, 11(10), 1424-1435 (2020-04-21)
Mesenchymal stem cells (MSCs) are of particular interest because of their potential in regenerative medicine. Stem cell-based therapies cast a new hope for neurodegenerative disease treatment as a regeneration strategy, including treatment for Alzheimer's disease (AD). A multitude of cytokines
Jing Wang et al.
Molecular medicine reports, 23(6) (2021-04-22)
Ginkgolide B (GB), the diterpenoid lactone compound isolated from the extracts of Ginkgo biloba leaves, significantly improves cognitive impairment, but its potential pharmacological effect on astrocytes induced by β‑amyloid (Aβ)1‑42 remains to be elucidated. The present study aimed to investigate the
Jingfu Zhao et al.
Neuroscience letters, 735, 135207-135207 (2020-06-28)
Alzheimer's disease (AD) is a dementing, neurodegenerative disorder characterized by increased accumulation of beta-amyloid peptides (Aβ), degeneration of hippocampal neurons and the gradual development of learning and memory deficits. Therapeutically, there are still no ideal medicines available and this represents

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