The presence of extracellular amyloid-beta plaques and tau neurofibrillary tangles has been a key neuropathological signature of Alzheimer’s disease (AD) in post-mortem analysis of patients. The generally accepted hypothesis is that pathological accumulation of toxic amyloid-beta peptides initiates the cascade of events leading to tau neurofibrillary tangles formation and to the progressive decline in cognition.
One of the initial areas involved in the Alzheimer’s pathology is the entorhinal cortex where tau pathology predominates. The general assumption has been that in the entorhinal cortex tau pathology precedes amyloid-beta pathology.
Contrary to the above widespread notion, the investigation of tau and A-beta amyloid signals in extremely well preserved brain material from aged, non-Alzheimer’s individuals, has challenged that established view. Thus, in a recent publication of Acta Neurolopathologica, doi: 10.1007/s00401-018-1922-z. [Epub ahead of print] (Welikovitch et al. 2018), a McGill team of researchers has been able to identify the progressive occurrence of intraneuronal amyloid beta accumulation in cortical AD-vulnerable regions of the brain prior to the occurrence of tau pathology.
The study was performed with a MediMabs’ well characterized anti-amyloid-beta antibody (MM-0015-P). MediMabs is proud in assisting scientists worldwide, facilitating discoveries by offering them high quality reagents and supporting them with our services.