a 23 amino acid peptide from near the carboxy-terminus of human presenilin1.
결합
The action of this antibody can be blocked using blocking peptide SBP4203.
물리적 형태
Solution in phosphate buffered saline containing 0.02% sodium azide
면책조항
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
Alzheimer's research & therapy, 12(1), 125-125 (2020-10-04)
Soluble beta-amyloid (Aβ) can be cleared from the brain through various mechanisms including enzymatic degradation, glial cell phagocytosis, transport across the blood-brain barrier, and glymphatic clearance. However, the relative contribution of each clearance system and their compensatory effects in delaying
Age (Dordrecht, Netherlands), 38(4), 303-322 (2016-07-22)
Transgenic APPSwe/PS1dE9 (APP/PS1) mice that overproduce amyloid beta (Aβ) are extensively used in the studies of pathogenesis and experimental therapeutics and new drug screening for Alzheimer's disease (AD). However, most of the current literature uses young or adult APP/PS1 mice.
Social isolation increases the onset of Alzheimer's disease (AD). Environmental enrichment, a complicated social and physical construct, plays beneficial effects on brain plasticity and function. This study was designed to determine whether physical enrichment can reduce the deleterious consequences of social
The imbalance between production and clearance of amyloid-beta (Aβ) is a key step in the onset and development of Alzheimer's disease (AD). Therefore, reducing Aβ accumulation in the brain is a promising therapeutic strategy for AD. The recently discovered glymphatic
Non-cognitive behavioral and psychological symptoms often occur in Alzheimer's disease (AD) patients and mouse models, although the exact neuropathological mechanism remains elusive. Here, we report hyperactivity with significant inter-individual variability in 4-month-old APP/PS1 mice. Pathological analysis revealed that intraneuronal accumulation