Fri, 06 Jun 2008 17:19:12 -0700, Michael Sylvester,PhD, wrote: >Any possibility that the brain eating amoeba can be conditioned to >eat away brain plaques and help alleviate diseases like Alzheimers?
Conditioning? I don't think so but then again I'm not an expert on current conditioing theory. However, I would speculate that there might be the possibility of genetically altering the amoeba to orient itself to plaques (with a specific genetic signature) instead of the usual components of the nervous systems which it attacks. >From the article on the emedicine website: http://www.emedicine.com/ped/TOPIC2807.HTM |Pathophysiology | |The events that lead to N fowleri-associated PAM usually result |from swimming or diving in warm water contaminated with N fowleri. |The N fowleri trophozoites enter the nose and invade the olfactory |mucosa, penetrate the submucosal nervous plexus, cross the |cribriform plate, and gain access to the subarachnoid space. |The presence of protein and glucose in the cerebrospinal fluid (CSF) |supports the growth of amebae, which then multiply rapidly and invade |the parenchyma of the brain. Because N fowleri possess mitochondria, |the high oxygen content of the brain and CSF enhance its growth. | |The invasive trophozoites are highly phagocytic and ingest RBCs and |brain tissue, resulting in severe hemorrhagic necrosis of the involved brain. |Brain tissue, unlike RBCs, cannot be ingested whole by the trophozoites; |however, N fowleri produces an amebostome, or food cup, into which |it secretes lysosomal hydrolases and phospholipases. N fowleri can also |use heat-stable hemolytic proteins, heat-labile cytolysin, phospholipase A, |and a cysteine protease to kill cells in contact with the trophozoites. |In 2000, Chu et al demonstrated that normal human serum is capable |of activating protein kinases with subsequent protein phosphorylation, |which results in enhanced complement resistance in N fowleri.4 | |N fowleri produces a diffuse hemorrhagic meningoencephalitis associated |with purulent meningitis. The cortical gray matter is the most severely |involved area. Because of severe edema of the brain, CSF pressures are |elevated, and uncal or cerebellar herniation can occur. | |Apart from the damage to the CNS, infection with N fowleri is also |associated with a neutrophilic myocarditis; however, amebic trophozoites |are not present in the myocardium. The clinical significance of this |myocarditis is unknown. | |The life cycle of N fowleri has 3 stages. | | 1. Trophozoite (vegetative) stage: The trophozoite is the reproductive |stage of the protozoan. The trophozoite measures 10-30 ¨m in diameter |and is characterized by a nucleus with a large centrally placed karyosome |with a surrounding halo. Trophozoites are motile and move by extending |a blunt lobopodium (pseudopodium) and allowing the cell cytoplasm and |contents to flow into the extension. Lobopodia form at different points |along the cell surface, allowing the trophozoite to change direction. In their |free state, trophozoites feed on bacteria and exhibit aerobic metabolism via |their mitochondria. In tissue, trophozoites phagocytize RBCs and WBCs |and destroy tissue with which they come into contact. Trophozoites replicate |by binary fission, which occurs only in this stage. | 2. Flagellate stage: When the N fowleri trophozoites are exposed to a |change in ionic concentration, such as placement in distilled water, they |transform into pear-shaped biflagellates or multiflagellates. | 3. Cyst stage: Trophozoites encyst in response to unfavorable conditions, |such as exposure to cold. The spherical cysts have a single nucleus surrounded |by a dense cell wall with 1-2 flat pores, which are plugged with mucus. Cysts |range from 7-14 ¨m. Betcha that's more than you wanted to know about naegleria fowleri. ;-) -Mike Palij New York University [EMAIL PROTECTED] --- To make changes to your subscription contact: Bill Southerly ([EMAIL PROTECTED])
