The following images are time-lapse pictures of a blood vessel in a mouse brain that has become blocked by debris. Watch the ingenious way the blood vessel rids itself of the blockage!

Time-lapse images of a blood vessel in a mouse brain. On Day 1, the interior membrane of the blood vessel starts to extend around the orange cholesterol blockage (arrow). By Day 3, the membrane has surrounded the cholesterol and created a pathway to the outside of the blood vessel (arrowhead). On Day 5, the blockage has moved outside the blood vessel, which is now unimpeded. (asterisk). Image courtesy of C.K. Lam, et al., Nature, 2010.

Tiny blood vessels in brain spit to survive

Time-lapse images of a blood vessel in a mouse brain.

On Day 1, the interior membrane of the blood vessel starts to extend around the orange cholesterol blockage (arrow).

By Day 3, the membrane has surrounded the cholesterol and created a pathway to the outside of the blood vessel (arrowhead).

On Day 5, the blockage has moved outside the blood vessel, which is now unimpeded. (asterisk).

Image courtesy of C.K. Lam, et al., Nature, 2010.

Spitting can be a good thing when it comes to blood vessels. Scientists at Northwestern University Feinberg School of Medicine have discovered capillaries have a unique method of expelling debris, such as blood clots, cholesterol or calcium plaque, that blocks the flow of essential nutrients to brain cells. The capillaries spit out the blockage by growing a membrane that
envelopes the obstruction and then shoves it out of the blood vessel.

Scientists also found this critical process is 30 to 50 percent slower in an aging brain and likely results in the death of more capillaries. "The slowdown may be a factor in age-related cognitive decline and may also explain why elderly patients
who get strokes do not recover as well as younger patients," said Jaime Grutzendler, senior author and principal investigator of the study and assistant professor of neurology and of physiology at Feinberg. "Their recovery is much slower."

The study with mice, funded by the National Institute on Aging (NIA), will be published May 27 in the journal Nature.

Scientists have long understood how large blood vessels clear blockages: blood pressure pushes against the clot and may eventually break it down and flush it away, or clot busting enzymes rush to the scene to dissolve a blockage. But very little was previously known about how capillaries clear blockages. The Northwestern study first demonstrated that enzymes and blood pressure aren't efficient at clearing capillary clots within the critical 24 to 48 hours. Those mechanisms only work half the time and only when blood clots are involved, not other types of debris, particularly cholesterol, which is difficult to dissolve.

"So what happens to the blood vessels that that aren't cleared out?" asked Grutzendler and colleagues. "Do they die, or does some other mechanism take over?" To find out, they created micro-clots, tagged them with a red fluorescent substance and infused them into the carotid arteries of mice. Using a multiphoton microscope, the team examined the brains of live mice at
various time intervals as clots traveled into the capillaries. Surprisingly, they discovered that the blood vessel cells next to the blockage grew a membrane that completely enveloped the debris. Then the original wall of the blood vessel opened up and spit the debris into the brain tissue, rendering it harmless. The envelope covering the clot became the new vessel wall. This resulted in complete restoration of blood flow and salvaging of the tiny vessel and surrounding brain cells.

"These are intriguing findings," said NIA director Richard J. Hodes, M.D. "They open new avenues of basic research that may increase our understanding of microvascular maintenance in the brain and throughout the body."

From PHYSORG.COM

Aging, brain function and memory loss are on the minds of every Baby Boomer in America. Millions of dollars are being spent on cosmetic surgery, organic food, brain training, exercise equipment and numerous other modalities that make us look and feel younger. So I thought it would be germane to mention a report I came across that reports the results of a new clinical study evaluating a "modernized" version of a previously helpful nutritional supplement called phosphatidylserine (PS). PS is a naturally occurring nutrient that lives in the membranes of cells. Approximately half of the PS in the body is located in the brain, much of it being in the mitochondria -- the power generating centers of each cell. When PS wears out it must be replaced or recycled.

Because of the vital roles played by PS, it was first made available as a nutritional supplement in the 1990s. At that time it was obtained from the brains of cows (the cerebral cortex) and was called BC-PS (Bovine Cortex PhosphatidylSerine). BC-PS is no longer on the market because of the risk of transmitting infectious agents such as the organism responsible for the production of Mad Cow Disease. PS supplements on the market today are derived from soy.

There was great interest in BC-PS because of the general medical support for its memory-enhancing properties. The PS currently available from soy doesn't generally share such robust clinical support. In fact, many of the products on the market have based their memory claims on the BC-PS literature. One might question whether those results can be applied to the soy-based PS. Many experts in brain research and alternative medicine have serious doubts about the validity of that leap of faith. Lloyd Horrocks, Professor Emeritus of Medical Biochemistry at the Ohio State University, believes "The fatty acids in BC-PS are mostly made up of DHA (docosahexaenoic acid -- an omega 3 fatty acid found in cold water fish) and arachidonic acid (an essential fatty acid in the omega 6 class) while the fatty acids from soy-derived PS are made mostly from oleic, linolenic and linoleic acids." Hence, the chemical composition of soy-derived PS is dramatically different from that of BC-PS, the product that was studied for cognitive benefits.

In addition to being chemically different, BC-PS is not pure phosphatidylserine. It is a mixture of many components of bovine cerebral cortex containing other fats. Thus, it is like comparing apples and oranges while evaluating soy PS and BC-PS. However, there is a new PS product on the market that has DHA complexed with a PS backbone making it much more biochemically like the BC-PS but without the risk of Mad Cow Disease. It is called PS-DHA and is manufactured by Enzymotec.

Scientific findings based on the usage of their novel form of PS-DHA were recently presented at a conference (the 25th Conference of Alzheimer's Disease International). The study was a double-blind, placebo-controlled trial that evaluated the efficacy of PS-DHA in healthy elderly individuals who had memory complaints but had not been diagnosed with Alzheimer's disease or any form of dementia. The dose tested was 300 mg of PS-DHA versus placebo. The trial period was 15 weeks. The Rey Auditory Verbal Learning Test and the Clinicians' Global Impression of Change scale were used. 53% of the patients in the PS-DHA group showed improved immediate recall (P=0.05) versus the placebo group. It was noted that the treatment was well-tolerated. The researchers concluded that PS-DHA had benefit and may improve short-term memory in this group of subjects.

This is a nutrient that should be evaluated by other scientists for similar cognitive benefits and might eventually be identified as a product that could be considered for inclusion in a supplemental program of brain health.

Alzheimer's disease is the most common form of dementia -- a progressive disease in which memory and thought processes become severely impaired.

Senile plaques are typical microscopic features seen in the brain tissue of patients with Alzheimer's disease. They are large aggregates of folded amyloid fibrils.  In 1985 amyloid beta was discovered. It is a chain of about 40-42 amino acids (the building blocks of proteins) linked end to end. Amyloid consists of clumps of this proteinaceous material.  As such, senile plaques have long been considered the primary killers of brain cells in this disorder. They were first discovered by Blocq and Marinescu in 1892. In 1906 Alzheimer first made the connection between plaques and dementia. In the 1970s M. Franke showed their association with dementing disease when the density of plaques in the frontal lobes was greater than 200/cubic millimeter. 

In the minds of researchers, the nexus between senile plaques and Alzheimer's disease became so entrenched that they were believed to actually cause the disease. Based on this theory of causation, medications were developed to remove the plaques. However, during drug trials designed to remove these plaques from the brain (such as the recent study testing bapineuzumab, which decreased plaques by 25%),  the patients' ability to think and reason got no better in spite of the decrease in plaques caused by the drug therapy.

This type of results have demonstrated to researchers that plaques are not the chief toxin responsible for Alzheimer's disease.  Moreover, not only are plaques not the cause of Alzheimer's disease, but it now appears that scientists are beginning to think they are a good thing!

According to Adrian Ivinson, director of the Harvard NeuroDiscovery Center in Boston, plaques actually appear to sequester all that amyloid. He went on to suggest that small particles of amyloid, called oligomers, rather than the large plaques, are the truly toxic substance. So it seems that like the capsule, or surrounding membrane, of a collection of pus, the plaque actually is protective rather than being the causative factor in Alzheimer's disease as has been believed all along. This insight has dramatically changed the way scientists view Alzheimer's disease and what they feel may be the optimal way to treat it.  I guess one take home message is that merely because something happens to share proximity with what causes a disease, it might not be the actual culprit.

It is worth taking a moment, in this context, to consider other diseases where related circumstances may have clouded scientific thinking in a similar fashion. Consider the cholesterol theory of heart disease. According to those who believe it, the build up of cholesterol in the blood somehow damages the arterial wall in very specific locations, in spite of the fact that the concentration of cholesterol is identical throughout the vascular tree. Could there be other factors that are producing injury to the lining membranes of blood vessels and that, once damaged, the cholesterol is deposited secondarily in the blood vessel wall in an attempt to repair the damage. If this is the case, then attention must be paid to other potential causes of vascular disease than cholesterol!