Journal of Alzheimers Disease & Parkinsonism
Open Access

Review Article

Neuronal Impulse Theory and Alzheimer's Disease

Helmut Barz^1*, Ulrich Barz² and Almut Schreiber³

¹Department of Pathology and Neuropathology, Dietrich-Bonhoeffer- Hospital, D-17022 Neubrandenburg, PF 400135, Mecklenburg-West-Pomerania, Germany

²Martin-Luther-Universität Halle-Wittenberg, Puschkinstrabe 12, D-06108 Halle, Saxony-Anhalt, Germany

³Consultant Occupational Health Physician, Institut für Arbeits- und Sozialhygiene, Aktiengesellschaft, Berg Str. 2, D-01096 Dresden, Saxony, Germany

Corresponding Author:

Helmut Barz
Department of Pathology and Neuropathology
Dietrich-Bonhoeffer- Hospital
D-17022 Neubrandenburg
PF 400135, Mecklenburg-West-Pomerania, Germany
Tel: 0049 038203 63309
E-mail: Helmut Barz@gmx.de

Received date: November 29, 2013; Accepted date: January 15, 2014; Published date: January 25, 2014

Citation: Barz H, Barz U, Schreiber A (2014) Neuronal Impulse Theory and Alzheimer’ s Disease. J Alzheimers Dis Parkinsonism 4:134.doi: 10.4172/2161-0460.1000134

Copyright: © 2014 Barz H, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

The paper gives a link to a mechanical hypothesis of the functioning and functionality of the brain. Mechanic impulses and pressure waves occur at the neuronal cell bodies and the neuronal fibers and conduct information. The requirement for these physiological aspects is a certain hydrostatic pressure in the neurons and an elasticity of the neuronal membranes. The alteration of the neuronal fiber walls due to the hydrostatic pressure in the neurons may be comparable with changes at the walls of arteries due to the blood pressure. In the older ages fiber breaks may occur with an escape of cytoplasm into the extracellular compartment and otherwise agglomerisation of the resting cytoplasm in the involved neuronal cell bodies. These two pathophysiological mechanisms may be important factors for the development of plaques and tangles.

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