Abstract

The paper based on the hypothesis that mechanical impulses cause the transmission of excitement in the peripheral and central nervous system. Possible connections between changes in the tubular neuronal network and the morphological findings of Alzheimer’s disease are presented.Additionally, changes in the viscosity of the neuronal cytoplasm and changes in the walls of the neuronal fibers due to the intracellular hydrostatic pressure and pressure waves are considered possible causes of plaques, threads and tangles. The pressure causes reduced elasticity and mechanical breakdown in neuronal fiber walls. This is compared to features found in blood vessels.It is presumed that damaged membranes lead to an escape of cytoplasm from the neurons into the extracellular space. This outflow may cause the spherical structured proteinaceous plaques. On the other hand it could be that the decrease of fluid and reduced intraneuronal pressure after a membrane crack may favor the agglomeration of cytoplasm proteins in the neurons forming threads and tangles. The consolidation of the neuronal cytoplasm and the irreparable decrement of the intracellular pressure cause a loss of function and finally a dieback of the affected neurons.The reduction of blood perfusion due to an increased local tissue pressure in certain regions of the brain may promote the forming of Alzheimer deposits. An increase of preamyloid proteins and small soluble amyloid particles within the extracellular fluid can lead, along their natural drainage route, to an amyloid angiopathy.

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