Neurons - The Computer Chips Of Our Brain

Brain Cells

The brain is the most complex computer nature has evolved and the neuron is the chip that makes that computer go. Like a computer, the brain also has electrical connections. These impulses have been programmed by life to interpret and control all that human beings do.

Neurons are a far more brilliant component than today's computers. They communicate not in ones and zeros, but more likely in a code as complicated as our alphabet. In a single brain region, neurons may have billions of connections with other neurons.

Neurons are cells of the brain that are responsible for information transfer, both within the neuron itself and between other neurons. A neuron has these components:

Axons - The Communication Links Of Neurons


Axons are the long protrusions from the cell body of a neuron that transmit out the signals of a neuron to other cells in the body. The axon is essentially the neuron’s electrical wire. The axon channels allow electronically charged chemicals to reach the terminal end, which then creates an electrical charge moving the electrical signal down to the "axonal bulb" at the end of the cell.

There is only one axon per cell, but the end is very complex and can make contact with other cells, usually other neurons, but sometimes muscle or gland cells. Axons are microscopically small, but they run throughout the brain and the nervous system in groups, called axonal tracts, which can be seen by the naked eye. Some axonal tracts can extend up to one meter or more while others extend as little as one millimeter. The longest axons in the human body are those of the sciatic nerve which runs from the base of the spinal cord to the big toe of each foot.

From the axon ends, the signal then crosses the "synapse" (the junction between two brain neurons) to reach the next cell. The positively charged ion will drain its charge as it moves to the synapse, where it will have its signal boosted again. Unlike electrical insulation, the axon coating is not a continuous coating, but contains individually separated small cells. Between each juncture of the axon, there is a small gap in the insulation called the Nodes of Ranvier. These gaps serve an important purpose allowing energy to enter the axon to boost the electrical signal as it traverses the length of the link.  Top

Glia Cells Are Critical For Neurons To Function

Types Of Glia

The defining characteristic of a neuron is its ability to transmit rapid electrical signals. All other neural cells that lack this property are categorized into a broad class called "glia".

Glia do not transmit action signals but instead surround and cover neuron cell bodies, axons and synapses throughout the nervous system. The human brain contains about nine glia cells for every neuron cell, i.e. our brains are 90% glia cells. Glia are essential to our brains, without them neurons die. There are three types of glia: oligodendrocytes, microglia, and astrocytes. Check out the purple, brown and green illustrations in the figure to the left.

The traditional view has been that glia look after neurons and maintain their proper functioning, having a somewhat passive role themselves. Established functions of glia include supporting neuro-transmission and insulating axons to speed up electrical communication. But resent research by Ben Barres and associates at Stanford University suggests that glia, particularly astrocytes, also have an "active role" in brain function and information processing.

Oligodendrocytes are the coatings on the cells that are spread end to end over the length of an axon. These glia cells resemble rolls of toilet paper, with the glia material wrapped many times around the core tube of the axon. Oligodendrocytes produce a non-soluble membrane called myelin, which wraps around axons and speeds up the conduction of electrical impulses.

Microglia, cells that fight diseases of the nervous system, survey the brain for any damaged and/or infected cells. They flow over and enclose all dead cells and debris. Microglia are also believed to be active during the development of the early nervous system removing inappropriate synaptic connections.

Astrocyte Photo

Astrocytes allow neurons to function. They contribute to a stable state of equilibrium in the brain by providing neurons with energy and substrates for neuron transmission. See the actual photo of an astrocyte cell (green) completely engulfing a neuron cell (orange) to the left.

Astrocytes act as physical barriers between the synaptic connections of neighboring neurons and remove excess neuro-transmitter molecules from the cellular space. This allows discrete and precise encoding of synaptic signals and neuro-transmission.

Recently, unexpected roles for astrocytes have been identified. They seem to be involved in the formation of synapses and in modulating synaptic functions through "bidirectional" communication with neurons.

Astrocytes control blood flow through their numerous processes which form close associations with blood vessels and neurons. In response to enhanced neuronal activity, astrocytes signal blood vessels the need for an increase in blood flow which then increases delivery of oxygen and glucose to an active brain region.

Besides regulating blood flow, astrocytes ferry glucose and oxygen from blood to neurons. It is hypothesized that they convert glucose into lactate. Lactate is then exported to neurons, where it is converted to pyruvate to produce the cell’s energy molecule ATP. Astrocytes communicate with each other through waves of calcium ions, propagating information over large distances. Stimulation of one astrocyte can cause a calcium response in a subset of neighboring astrocytes, with no response in other subsets. Bidirectional communication also occurs between neurons and astrocytes. Individual astrocytes can make contact with and cover up thousands of synapses formed between different neurons.  Top

Our Brain Resets During Sleep

Brain Neurons

Researchers at the University of Wisconsin School of Medicine have tested a theory called Synaptic Homeostasis Hypothesis (SHY) for why humans need sleep. The four year study was published in the February, 2017 issue of Science magazine. SHY theory describes changes in synapses during waking and sleeping hours. See the illustration to the left. The large globs are neurons and the synapses are the junction connections (glowing white) between neurons. Our synapses grow strong and large during the stimulation of daytime, then shrink by nearly 20 percent while we sleep, creating room for more growth and learning the next day.

The larger the synapse, the stronger two neurons communicate. This ease of communication is how humans learn skills and retain memories. In order for brains to be pliable and learn new things, the synapses must shrink so the neural pathways can be activated again. According to SHY theory, sleep provides the environment for the shrinking of synapses allowing the brain to learn new things the following day.

The lack of stimulation while sleeping results in reduced activity between neurons. The size of the synapse grows smaller allowing them to be activated with a weaker stimulation. This phenomenon allows brains to make new neural connections the following day, thereby allowing new memories to form.

Researchers tested the SHY theory by measuring the size of synapses in a mouse study both before and after sleep. They utilized a three-dimensional scanning electron microscopy to reconstruct the mouse brain and measured about 7,000 synapses. They specifically looked at neurons involved in motor functions and sensory perception. The team then repeated this process after the mice had slept and measured the synapses again.

The researchers found that the synaptic size correlated with the amount of sleep the mice had. The longer the mice slept, the smaller the synapses had become – with a few hours sleep resulting in a reduction of about 18 percent. Interestingly, the researchers only observed this phenomenon in about 80 percent of the synapses and that the largest of synapses appeared not to be susceptible to shrinking. They hypothesize that these large synapses might not follow the pattern because these synapses are associated with stable, long term memories and/or skills.

The results support SHY’s central tenant that the function of sleep is to re-normalize synapse size that increases throughout the day. The researchers theorize that the shrinking of the synapses might be related to the lack of neuro transmissions during sleep. The takeaway: Getting seven hours of sleep every night keeps human brains healthy.  Top

Brain Derived Neurotrophic Factor (BDNF Gene and BDNF Protein)

BDNF Brain

“Researchers at the Rush Alzheimer’s Disease Center in Chicago, Illinois reported intriguing evidence that people with higher levels of a nerve growth factor called BDNF tended to keep more of their cognitive functions even as amyloids built up. In fact people who had more BDNF activity saw 50% slower rate of cognitive decline over the study’s six years than those with lower BDNF activity” (Time Magazine, Feb 2016).

The BDNF gene provides instructions for making a protein found in the brain and spinal cord called brain-derived neurotrophic factor, also called BDNF for short. Although related, one BDNF is a gene and the other BDNF is a protein. The protein promotes the survival of nerve cells (neurons) by playing a role in the growth, maturation, and maintenance of the nerve cells. As a neuroprotein, BDNF is responsible for growing new neurons and repairing broken ones.

In the brain, the BDNF protein is active at the connections between nerve cells (synapses), where cell-to-cell communication occurs. The synapses can change and adapt over time in response to experience, a characteristic called synaptic plasticity. The BDNF protein helps regulate synaptic plasticity, which is important for learning and memory.

The BDNF protein is found in regions of the brain that control eating, drinking, and body weight; the protein likely contributes to the management of these functions.

With a growing body of scientific evidence, it is no wonder that brain derived neurotrophic factor (BDNF) is quickly becoming one of the hottest compounds in brain health.

For decades, scientists have pursued an Alzheimer's cure with a single minded focus on how to treat the disease - get rid of the hallmark feature of Alzheimer’s which is the sticky protein plaques of amyloid (this has been very sucessful in mice). However, since 2000 more than 200 Alzheimer’s drugs have been tested, and none has proved to be a winner. Several drug companies have stopped trying and have cancelled all research projects. The situation is further confused by the fact that perfectly normal people also have some amyloid and tau plaque build up. Are the plaques really the enemy? Maybe BDNF is a solution - promote healthy nerve cells and live with the plaques.

Exercise is the most commonly known way of increasing BDNF, but people have also started looking towards other ways that they can increase this key protein for brain health. Unfortunately, many of the supplements that are touted for having the ability to increase BDNF, come up short due to the lack of research in humans (mice are frequently studied, but many results do not apply to humans).

Here are 4 supplements that "may" increase BNDF levels in your body.

1. Fish oil -There are several studies in animals that show when researchers induce dramatic brain injuries, the addition of omega-3 fats (like those found in fish oil) help to normalize levels of BDNF in these animals. Unfortunately, there are no human studies showing that taking a fish oil supplement will increase BDNF levels.

2. Curcumin - Curcumin, an extract from turmeric, is known for its anti-inflammatory properties, but some animal research suggests that curcumin can play a role in increasing BDNF levels. In one study, researchers took brain cells from mice and treated them with curcumin. This treatment with curcumin led to increases in BDNF levels. Unfortunately, there are no human studies showing that supplementing with curcumin will increase levels of BDNF.

3. Cocoa - Cocoa is known to be a powerful antioxidant. Research from Sbarro Institute for Cancer Research and Molecular Medicine, and the Center for Biotechnology at Temple University shows that cells that behaved as if they were inflicted with Alzheimer's disease were treated with antioxidants from cocoa. They found that the cocoa antioxidants turned on the cell's protective mechanism by activating the BDNF survival pathway. This research is very interesting, however, it is still a stretch to say that consuming cocoa will lead to increases in BDNF.

4. Coffee Fruit (NeuroFactor™) - The fruit from a coffee plant contains a powerful blend of antioxidants. The concentrated form of these antioxidants, called NeuroFactor™, has been shown - in two separate clinical studies - to increase BDNF levels in humans in less than 2 hours. This is the only supplement which has been clinically shown to increase BDNF levels in humans.

As you can see from the first three supplements above, there may be a plausible cellular mechanism for some of them to increase BDNF, but their ability to do so in humans has yet to be proven.  Top

DHA Keeps Our Brain Healthy

DHA Brain

DHA (docosahexaenoic acid) is an omega-3 fatty acid found in fish oils that plays a central role in brain health. DHA is naturally found throughout the body, but is most abundant in the brain. Our brain is mostly fat, of which 60% is DHA. Just as calcium is essential for building strong bones, DHA ensures that the cells in the brain and other parts of the nervous system develop and function properly through all stages of life.

DHA not only turns on the growth of new brain cells, but offers protection for existing brain cells while it enhances the ability of one brain cell to connect to the next. DHA also acts as an anti-inflammatory. This is quite significant when one recognizes that inflammation is a key factor in both Alzheimer’s as well as Parkinson’s disease. And, DHA is active in controlling virtually every other neuro-degenerative condition.

DHA Pills

A research team from the New Orleans School of Medicine in an April 2017 paper explained how DHA helps a damaged brain recover and keeps it functioning. Neuroprotectin D1 (NPD1) is a lipid messenger made from DHA on demand when cell survival is compromised. Oxidative stress, resulting from the constant production of damaging free radicals, lays the groundwork for cell death. Cell death is accelerated by catastrophic events like ischemic stroke.

The team found that about one hour after an experimental stroke, DHA triggered the production of NPD1. NPD1, in turn, increased the production of ring finger protein 146, which has been named Iduna. Iduna protects against a form of programmed cell death from stroke. Iduna, relatively little studied, turns out to be a key factor for cell re-programing and subsistence.

DHA is available as a supplement derived from fish oils as well as from marine algae. See the photo to the left. There is DHA in krill oil but the amount of DHA in krill oil is only about 10% of that found in fish oil. Eating fatty wild fish is a good source of DHA and clearly explains why fish is considered a “brain food.” DHA can be found in stores as a non-prescription supplement and can be purchased from Life Extension here.  Top

Deep Brain Stimulation (DBS)

Deep Brain Stimulation

Deep Brain Stimulation, DBS, involves surgery for the implantation of electrodes deep inside the brain and then an electrical pulse generator sends stimulation pulses to the target area via microwires (the idea is similar to a heart pacemaker). This procedure was first introduced in 1987 on an experimental basis and was approved by the FDA in 1997 for treating Parkinson's Disease. About 150,000 Parkinson’s patients around the world have received an implant.

To treat Parkinson’s, the electrodes are placed in a brain region involved with movement. While the detail mechanisms of a DBS implant are still not clear, many researchers think the steady stimulating pulses override faulty patterns of normal electrical activity in certain regions of the brain.

DBS is currently being implemented on a very small sample of patients with "severe depression" on an experimental basis. For depression much research has centered on finding the proper targets for stimulation. The problem is that experimental trials have consistently had a subset of people who simply don’t respond to the treatment. So at this time, it has not been formally approved for severe depression any place in the world.

Recently at research center Emory University in Atlanta, 11 patients with severe depression who hadn’t responded to drugs, talk therapy, or electro-convulsive therapy, were given the DBS treatment. When all the patients were evaluated six months later, 8 of the 11 were judged to be responding well to the treatment. For one of the non-respondents, the researchers adjusted the parameters to better match the desired area of fiber activation. He got better quickly. Those that have had positive results stay better for very long periods of time - so far up to 10 years. For the two who did not respond, rearchers say depression is a complicated syndrome. There are probably some factors beyond the brain that need to be addressed.

In Germany, there is a 50-patient severe depression study expected to begin DBS implantations in the second half of 2017. If the results of this three-year trial are good, researchers believe that DBS treatment for depression will be on the path to regulatory approval in Europe. In the United States, regulatory approval requires a much more rigorous trial. Stay tuned.  Top

Alheimer's Association Recommendations

10 Ways to Love Your Brain. Growing evidence indicates that people can reduce their risk of cognitive decline by adopting key lifestyle habits. When possible combine these habits to achieve maximum benefit for the brain and the body. Start now. It’s never too late to incorporate healthy habits.

Break a sweat.
Engage in regular cardiovascular exercise that elevates your heart rate and increases blood flow to the brain and body. Several studies have found an association between physical activity and reduced risk of cognitive decline.
Hit the books.
Formal education in any stage of life will help reduce your risk of cognitive decline and dementia. For example, take a class at a local college, community center or online.
Butt out.
Evidence shows that smoking increases risk of cognitive decline. Quitting smoking can reduce that risk to levels comparable to those who have not smoked.
Follow your heart.
Evidence shows that risk factors for cardiovascular disease and stroke — obesity, high blood pressure and diabetes — negatively impact your cognitive health. Take care of your heart, and your brain just might follow.
Heads up!
Brain injury can raise your risk of cognitive decline and dementia. Wear a seat belt, use a helmet when playing contact sports or riding a bike, and take steps to prevent falls.
Fuel up right.
Eat a healthy and balanced diet that is lower in fat and higher in vegetables and fruit to help reduce the risk of cognitive decline. Although research on diet and brain function is limited, some diets like the Mediterranean and DASH diets, contribute to risk reduction.
Catch some Zzz's.
Not getting enough sleep due to conditions like insomnia or sleep apnea may result in problems with memory and thinking.
Take care of your mental health.
Some studies link a history of depression with increased risk of cognitive decline, so seek medical treatment if you have symptoms of depression, anxiety or other mental health concerns. Also, try to manage stress.
Buddy up.
Staying socially engaged may support brain health. Pursue social activities that are meaningful to you. Find ways to be part of your local community — if you love animals, consider volunteering at a local shelter. If you enjoy singing, join a local choir or help at an afterschool program. Or, just share activities with friends and family.
Stump yourself.
Challenge and activate your mind. Build a piece of furniture. Complete a jigsaw puzzle. Do something artistic. Play games, such as bridge, that make you think strategically. Challenging your mind may have short and long-term benefits for your brain.


"Reversing" Alzheimer's Disease

Cheaing Death

In 2012 researchers from UCLA and the Buck Institute for Research on Aging announced the results of a "first ever" study in which nine out of 10 subjects diagnosed with dementia saw meaningful "reversals" of memory loss. This study is of particular significance to those already suffering from early to mid-stage Alzheimer’s.

The approach used in the UCLA/Buck Institute study was personalized to each patient based on extensive testing to determine what is affecting the brain’s plasticity signaling network.

The one patient that failed to show improvement was unable to comply with all of the components of UCLA/Buck Institute protocol. Nine out of 10 people in this study who did comply showed "reversals" in measurements of memory loss.

The UCLA/Buck Institute study author, Dr. Bredesen, admitted however, that the program’s downside is its complexity. While supplementing with melatonin, fish oil, coenzyme Q10, methylcobalamin, and vitamin D3 were easy, the dietary/lifestyle changes were so difficult that none of the 10 participants were able to stick to the entire protocol.

Here is a sample of some of the strategies used in the therapeutic program to reverse memory loss:

Follow On Testing Of A Larger Population

Smiling Man

An obvious criticism of the initial 2012 study above is the small number of patients involved - only 10. Therefore, a follow on study was completed on 100 patients, treated by several different physicians, with "documented" improvements in cognition. The paper was published in October, 2018 in the Journal of Alzheimer’s Disease.

Alzheimer’s disease is now the third leading cause of death in the United States, and the development of effective treatment and prevention is a major healthcare goal.

However, clinical trials of drug candidates for Alzheimer’s disease treatment have been uniformly unsuccessful (more than 200 Alzheimer’s drugs have been tested, and there have been no winners).

There probably are several reasons for the repeated failures:

In the follow on test the patients with cognitive decline were treated with a multiple approaches and precision medicines, resulting in documented Alzheimer's improvement in 72 of the 100 patients (an amazing 72%). For those evaluated by the Montreal Cognitive Assessment (MoCA) or other similar tests, there was a mean improvement of 4.9 points, with a standard deviation of 2.6. (MoCA scores range between 0 and 30. A score of 26 or over is considered to be normal. In a recent study, normal people scored an average of 27.4; people with mild cognitive impairment (MCI) scored an average of 22.1; people with Alzheimer's disease scored an average of 16.2.)