Compensatory mechanisms to heal neuroplasticity impairment under Alzheiemer's disease neurodegeneration. I: The role of amyloid beta and its' precursor protein

In-depth scholar literature analysis of Alzheimer's disease neurodegenerative features of amyloid beta protein neurochemistry modification and excessive phosphorylation of tau protein (and associated neuronal cytoskcleton rearrangements) are secondary phenomena. At early disease stage these neurobiochemical mechanisms arc reversible and serve to heal an impairment of biophysical properties of neuronal membranes, neurotransmission, basic neuronal function and neuroplasticity, while preserving anatomical and functional brain fields. Aβ and tau could well serve to biochemically restore physico-chemical properties of neual membranes due to a role these proteins play in lipid metabolism. Under such scenario therapeutic block of aggregation and plaque formation of Aβ and inhibition of tau phosphoiylation, as well as pharmaceutical modification of other secondary neurodegenerative features (such as a cascade of oxidative stress reactions) arc unable to provide an effective cure of Alzheimer's disease and related pathologies of the Central and peripheral nervous systems, because they are not arraying primary pathagcnctic cause. We review the role of Aβ in compensatory mechanisms of neuroplasticity restoration under normal physiological condition and Alzheimer's disease.