Pressure waves in neurons and their relationship to tangled neurons and plaques

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.

Modelling of processes in nerve fibres at the interface of physiology and mathematics

“…In what follows, an attempt is described following the ideas of Andersen et al [2] to build up a mathematical model which could account for main effects in signal propagation in nerve fibres. Based on classical understandings of axon physiology [9,12], the following basic assumptions are made: (i) electrical signals are the carriers of information [12] and trigger all the other processes; (ii) the axoplasm in a fibre can be modelled as fluid where a pressure wave is generated due to electrical signal; here, for example, the actin filaments in the axoplasm may influence the opening of channels in the surrounding biomembrane but do not influence the generation of pressure wave in the fluid [2]; (iii) the biomembrane is able to deform (stretch, bending) under mechanical impact [24]; (iv) the channels in biomembranes can be opened and closed under the influence of electrical signals as well as of the mechanical input; it means that tension of a membrane leads to the increase of transmembranal ion flow and the intracellular actin filaments may influence the motions at the membrane [4,32]; (v) there is strong experimental evidence on electrical or chemical transmittance of signals from one neuron to another [5,26] although the role of mechanical transmission is also discussed [3].…”

Reliability bounds for two dimensional consecutive systems

“…Some explaination is still needed on how the brain takes advantage of pressure waves, temperature and concentration gradients to allow the renewal of the extra-cellular fluid, as well as some forms of intercellular communications at an energy cost way lower than the well-established synaptic transmission [1]. One alternative discusses solitons in the context of mechanical dislocations and temperature changes [25,23,24], while others suggested an axoplasmic pressure pulses [43,4], or electromagnetic pulses [49]. In fact, many studies have shown that a mechanical displacement of the axonal membrane accompanies the electrical pulse which has been used to define an action potential, but there is little theoretical consensus for the physical basis of such waves or their links with the electrical pulse.…”