APP抗体

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     Black line: Control Antigen (100 ng); Purple line: Antigen(10ng); Blue line: Antigen (50 ng); Red line: Antigen (100 ng);    

  
  

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     Immunofluorescence analysis of A431 cells using APP mouse mAb (green). Blue: DRAQ5 fluorescent DNA dye. Red: Actin filaments have been labeled with Alexa Fluor-555 phalloidin. Secondary antibody from Fisher (Cat#: 35503)    

  
  

APP (amyloid precursor protein) is a transmembrane glycoprotein highly expressed in the brain and involved in synaptic formation, neuronal plasticity, and intracellular signaling. Its proteolytic processing through amyloidogenic or non-amyloidogenic pathways plays a central role in Alzheimer’s disease (AD) pathogenesis. In the amyloidogenic pathway, sequential cleavage by β-secretase (BACE1) and γ-secretase generates neurotoxic amyloid-beta (Aβ) peptides, which aggregate into plaques—a hallmark of AD. APP-targeting antibodies have emerged as critical tools for both research and therapeutic exploration.

Research-grade APP antibodies are widely used to detect APP expression, localization, and processing in cellular and animal models (e.g., transgenic mice), as well as in human biofluids like cerebrospinal fluid (CSF). These antibodies often target specific APP epitopes (e.g., N-terminal, C-terminal, or Aβ domains) to distinguish full-length APP from its proteolytic fragments (e.g., sAPPα, sAPPβ, Aβ). Therapeutically, anti-Aβ antibodies (e.g., aducanumab, lecanemab) aim to clear Aβ plaques or neutralize soluble Aβ oligomers, with some achieving clinical approval despite ongoing debates over efficacy and safety. Other strategies include BACE1 inhibitors or antibodies targeting APP cleavage sites to modulate Aβ production. Challenges remain in optimizing blood-brain barrier penetration, minimizing off-target effects, and addressing the complex pathophysiology of AD beyond Aβ-centric approaches. APP antibodies thus represent a dual-purpose innovation, bridging mechanistic studies and therapeutic development in neurodegenerative research.