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How malaria’s effects on the brain kill millions October 1, 2006

Posted by Hegemony in Science.
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Malaria is one of the most prevalent diseases in the tropical and sub tropical world. It is caused by infection with parasites of the genus Plasmodium. In addition to the common symptoms there is also the possibility of developing Cerebral Malaria. This is a rare occurrence but accounts for over two million deaths a year in children under 5 years of age. Examination of the brain tissue of diseased individuals shows blockage of brain microvessicles. These blockages are composed primarily of host platelets and Plasmodium infected red blood cells, sometimes with the presence of leukocytes. The damage to the brain can only be studied in deceased human patients. However, the use of a Murine (mouse) model illustrates the course the disease is likely to take in humans.

The breakdown of the blood brain barrier is key to the pathogenesis of the disease. The mouse model implicates the host platelets as having a key role in this. There are three possible ways that platelets can alter the blood-brain barrier (endothelial cells). They can secrete inflammatory mediators like IL-1, affect leukocytes directly, and congregate with infected red blood cells forming clumps. To study this interaction more thoroughly the authors developed an in vitro model of a cerebral malaria endothelial lesion. The findings corresponded with what was known about the pathogenesis in humans. Platelets were found in higher levels in the brain microvessicles of those that died of cerebral malaria. Platelets express large amounts of CD36 on their surface. This protein is known to assist in the binding of the platelet-infected RBC aggregate to endothelial cells. These observations indicate a definite role for platelets in the pathogenesis of cerebral malaria. The accumulation of these cells in brain micovessicles may contribute directly to the microvascular damage.

Microparticles have also been implicated in the disease process. Microparticles are phospholipid micro vesicles containing cell surface proteins from their parent cell. These are released during membrane rearrangement and vesiculation in eukaryotic cells. Plasma samples from individuals with acute cerebral malaria indicated far higher levels of endothelial microparticles than are present in a standard malaria infection. These levels also correlated to increased levels of TNF, which is known to increase the release of endothelial microparticles.

In a mouse model using knockout mice deficient in ABCA1 (a protein relating to erythrocyte vesiculation) the disease process was tracked. The mice lacking ABCA1 had no legions and did not contract cerebral malaria. Levels of TNF and microparticles were also much lower in the experimental mice as compared to the control group. This seems to indicate that microparticles are involved as with decreased vesiculation comes less microparticle production. While it can not yet be proposed that microparticles have a definite role it seems possible as we know they can act as effector molecules. Additional tests show that microparticles from the control animals caused more clotting than the microparticles from the knockout mice.

These discoveries could result in new therapies for cerebral malaria. If the cell to cell interactions of platelets and infected red blood cells could be lessened it would likely result in resistance to the breakdown of the blood-brain barrier. In addition microparticles may also be targeted. The decrease in microparticles in knockout animals seemed to protect them from the neurological symptoms.

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Comments»

1. NA - November 16, 2007

Can you make it a bit easier to understand?

2. Hegemony - November 18, 2007

No… there are some articles here I’ve written in a more scientific way (like this one), and some that I’ve tried to make more accessible. This article assumes familiarity with at least high school level biology. If I tried to write about this in a more accessible way I’d have to explain too many terms and such.

3. salman ashraf - September 9, 2009

my friend is suffering from this disease

4. justine - July 22, 2010

hi, i use to have celebral malarial when i was very much young, but was treated by the age of 10, now am 27, i suffer from severe brain fatigue even when am not studying or have my brain worked up. When it started, i use to think i needed rest, but i can have ample rest and even sleep, but the moment am up, am back to it. A friend told me it could be the effect of celebral malarial. Could that be the case?

nitish - March 6, 2012

it may be friend….but i am not sure ..but same symptoms are happening with my friend who is suffering with same symptoms and result came as brain malaria….

5. justine - July 22, 2010

if yes, how do i go about it pls

6. Leslie R. Carlson - January 29, 2012

My daughter-in-law is from Brazil, now in Canada. She was infected
during childhood three times. Recently she has shown bizarre behavior ie temper tantrums, threatening to leave, inability to get along with anyone, unusual suspicions about other people, and she shows signs of depression, she cannot sleep, is exhausted all the time and becomes hot and cold constantly. Her usual sweet disposition is gone. Could malaria be affecting her brain? My son is distraught and doesn’t know what to do. She is only 27 years old.

Leslie Jan. 29. 2012

7. Wasim - July 22, 2012

Hi all, my son also infected with this fever, he is just 1 and half year old, i’m very scared about it & doctor has advise syrup MATCH-Q every day night 10ml, does it really works for brain maleria..? pls help me to save my son

8. victor - August 4, 2012

how to test maleria, brain maleria, typhoid & Dengo?

9. Aldea - February 27, 2013

A relative died in a penal colony at Cayenne in 1905. The cause of death was celebral malaria. Were doctors in those days knowledgeable enough to determine the exact cause…was it based on sympthoms only?


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