During the past dozen years, a steadily accumulating body of evidence has indicated that soluble forms of Aβ and tau work together, independently of their accumulation into plaques and tangles, to drive healthy neurons into the diseased state and that hallmark toxic properties of Aβ require tau. The behavioral symptoms of Alzheimer’s disease(AD) correlate with the accumulation of plaques and tangles, and they are a direct consequence of the damage and destruction of synapses that mediate memory and cognition.
Tau(10E3) Monoclonal Ab
Tau is a brain-specific, axon-enriched microtubule-associated protein and plays a primarily role in maintaining the stability of microtubules in axons and is abundant in the neurons of the central nervous system (CNS).
Amyloid-β polyclonal Ab
Amyloid-beta peptides are the main component of the amyloid plaques found in the brains of Alzheimer’s disease patients. Aβ plays a critical role and may be an upstream molecule in AD pathogenesis.
BT LAB’s antibodies for Alzheimer’s disease research