United States: New published research from the University of Cincinnati begs to produce traditional notions of handling Alzheimer’s disease. Scientists discovered that new kinds of drugs known as monoclonal antibodies may protect memory loss by increasing amyloid-beta 42 (Aβ42) in the brain in addition to an earlier belief of decreasing the plaques. This discovery gives the implication that Aβ42 could have a special function of maintaining the brain health.
Alzheimer’s disease is a form of dementia and the most common form of dementia that introduces itself by symptoms of forgetfulness, gradual decline in mental capacity, and Social/Psychological alterations. The disease gradually impairs patient’s functions, reduces their quality of life, and is now present in millions of patients world-wide.
As reported by the PsyPost, At a biological level, Alzheimer’s is marked by two main features: amyloid lesions in extracellular form and the intracellular neurofibrillary tangles of tau protein.
Amyloid-beta is a peptide, which is generated in the brain under normal physiological processes of cellular turn over.
It is present in varying forms; however, more importance is placed on two variants, amyloid β-40 and amyloid β-42 in Alzheimer’s disease. A β 40 is the most common peptide constituting 90 percent of total A β generated and is not cytotoxic in normal concentrations.
However, while Aβ42 is less prevalent than unprocessed-ed Aβ40, it is more likely to aggregate and build up in plaques.
Due to this enhanced aggregation propensity, Aβ42 has emerged as the central experimental model for Alzheimer’s disease pathogenesis.
The amyloid cascade hypothesis has remained the belief of choice since early 1990s, the change was proposed that indicated 10 years of pathological research. This theory argument brings into the limelight the fact that Alzheimer’s starts with the aggregation of Aβ42 molecules to form oligomers.
These oligomers stack to form insoluble amyloid plaques which are used to interfere with neuronal signaling, provoke inflammation, and cause the extensive neuronal pathology evident in Alzheimer’s. Backing up this hypothesis, for example, the genetic investigations proved that the changes in genes regulating the creation of amyloid are associated with the existence of the rare hereditary form of Alzheimer’s disease.
Arizona Neurology professor Alberto J. Espay and his team speculated that sticky, insoluble Aβ42 would not spread in brains, rather the absence of normal soluble Aβ42 might contribute to Alzheimer’s disease. Evidence for this is provisional but one multiparametric study has indicated that Aβ42 has a vital function in the integrity of neurons and in the function of synapses. Conversely, the loss of HDAC2, its absence rather than accumulation, may result in cognitive dysfunction.