Peter Wostyn*, Kurt Audenaert and Peter P De Deyn
Corresponding author: Peter Wostyn email@example.com
Cerebrospinal Fluid Research 2009, 6:14 doi:10.1186/1743-8454-6-14
(2010-11-03 17:58) University of Pittsburgh
The current research on Alzheimer’s disease is primarily focused on the discovery
of specific protein subunits as well as identification of genetic mechanisms involved
in this disease. With the appearance of the “hypoperfusion” theory as
well as findings from numerous population-based studies linking Alzheimer’s
disease to “vascular” disorders (i.e. hypertension, atherosclerosis etc.)[1,2],
it became evident that the important task for understanding Alzheimer’s disease
is to thoroughly examine local fluid (i.e. cerebrospinal) dynamics. Such approach
may also result in finding of successful treatments of Alzheimer’s disease.
One of the mechanisms that can describe, for instance, an association between cardiac
pathology (i.e. cardiac arrhythmia) and Alzheimer’s disease is the disturbances
in the dynamics of regional brain extravascular extracellular fluid. Such consideration
of regional brain extravascular extracellular fluid dynamics is also particularly
important in light of the fact that certain waste products such as glutamate or calcium
can accumulate there causing degradation of certain cellular components thus playing
an important role in the pathogenesis of Alzheimer’s disease[4,5]. Such mechanism proposes that the regional brain extravascular extracellular fluid
gets moved due to the cyclic changes in the vessel wall deformation, a sort of a “deformation
pump”. The operating principle of the “deformation pump” is in
the cyclic creation of the boundary layer and in its separation. Thus the movement
of the regional brain extravascular extracellular fluid happens as a result of the
appearance and separation of the boundary layer at the close proximity to the vascular
wall. The obvious implication of this mechanism is the primary involvement of cardiovascular
system in the development of Alzheimer’s disease. Rovshan M Ismailov, M.D., M.P.H., Ph.D. References  de la Torre JC. Impaired brain microcirculation may trigger Alzheimer's disease.
Neurosci Biobehav Rev 1994; 18(3):397-401.  de la Torre JC. Cerebral hypoperfusion, capillary degeneration, and development
of Alzheimer disease. Alzheimer Dis Assoc Disord 2000; 14 Suppl 1:S72-81.  Ismailov RM. New insights into the mechanism of Alzheimer's disease: A multidisciplinary
approach . edn. Amazon Kindle, 2010.  Mattson MP. Calcium as sculptor and destroyer of neural circuitry. Exp Gerontol
1992; 27(1):29-49.  Khachaturian ZS. The role of calcium regulation in brain aging: reexamination
of a hypothesis. Aging (Milano) 1989; 1(1):17-34.
I declare no competing interests
BioMed Central Ltd unless otherwise stated. Part of Springer Science+Business Media.