Email updates

Keep up to date with the latest news and content from Fluids and Barriers of the CNS and BioMed Central.

Open Access Highly Accessed Open Badges Commentary

More advanced Alzheimer's disease may be associated with a decrease in cerebrospinal fluid pressure

Peter Wostyn*, Kurt Audenaert and Peter Paul De Deyn

Cerebrospinal Fluid Research 2009, 6:14  doi:10.1186/1743-8454-6-14

PubMed Commons is an experimental system of commenting on PubMed abstracts, introduced in October 2013. Comments are displayed on the abstract page, but during the initial closed pilot, only registered users can read or post comments. Any researcher who is listed as an author of an article indexed by PubMed is entitled to participate in the pilot. If you would like to participate and need an invitation, please email, giving the PubMed ID of an article on which you are an author. For more information, see the PubMed Commons FAQ.

Fluid dynamics and Alzheimer's disease

Rovshan Ismailov   (2010-11-03 17:58)  University of Pittsburgh email

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[3]. 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”[3]. 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.


[1] de la Torre JC. Impaired brain microcirculation may trigger Alzheimer's disease. Neurosci Biobehav Rev 1994; 18(3):397-401.
[2] de la Torre JC. Cerebral hypoperfusion, capillary degeneration, and development of Alzheimer disease. Alzheimer Dis Assoc Disord 2000; 14 Suppl 1:S72-81.
[3] Ismailov RM. New insights into the mechanism of Alzheimer's disease: A multidisciplinary approach . edn. Amazon Kindle, 2010.
[4] Mattson MP. Calcium as sculptor and destroyer of neural circuitry. Exp Gerontol 1992; 27(1):29-49.
[5] Khachaturian ZS. The role of calcium regulation in brain aging: reexamination of a hypothesis. Aging (Milano) 1989; 1(1):17-34.

Competing interests

I declare no competing interests


Post a comment