Brain development and function

If the brain of a newborn child was completely empty, it would probably be very difficult for the mind to get started after birth. But we, who have had several new-borne babies in the family, know that it is possible to obtain contact rather early. Moreover, the child’s personality is recognized early in the first year of life. Therefore, one must assume that there is an innate memory that may be called basic memory. When the baby smiles in recognition of mom’s or dad’s smacking or gurgling sounds, it is assumed that a memory that includes these sounds probably is present already and is activated and recognized when the sounds occur. It is such simple sounds, not complicated ones, which seem to trigger an innate memory of the small baby.

If one accepts that this part of the memory is innate, we can continue. It certainly is a big difference between the immunological memory and the brain’s memory, but also similarities since many brain cells are derived from bone marrow and antibodies can be produced in the brain.

At birth the immune system contain millions of kinds of antibody producing cells. Since there are so many kinds, each kind will only include few cells. If one antigen e.g. red sheep blood cells are injected into a mouse, the few innate immune cells of this kind will multiply and give a lot new identical cells even within 5 days. This growth of immune cells will be inhibited in a dose dependent way if the mice receive Invasivol simultaneously.

Since no specific immune organ is described in the brain, it must be some of the brain cells themselves that produce antibodies inside the blood/brain barrier during infection of the brain. Such immune cells can probably divide and monocytes can transport infectious agents to the brain e.g. HIV. Since such cells can transport an infection they may also be able to pass through without infection.

If the hypothesis of the existence of an innate basic memory is true, the basic associations are probably small and may therefore be inactivated relatively soon by the postulated specific clone inhibitors. Then there has to be a renewal of these cells. The most likely possibility may be renewal by cells from the bone marrow where such cells probably are produced continuously along with the true immunological ones.

In addition to the above mentioned recognition of simple sounds etc., there may also be basic memory in other areas such as the emotional, ethical, proprioceptive and perhaps religious field. Each of these basic memories is believed to be related to specific cells similar to those carrying the memory of the immune system.

But why cannot the child remember from its first year of life and maybe not from its second or third year either?

The first small associations will probably be memorized longer if they increase their size and form middle sized and great associations. Then they will be remembered for longer time; for weeks, months or years. But this process may take several months or a few years.

The brain’s neurons are assumed to contribute in establishing synaptic connections with other brain cells that have similar properties.  Neuroglia may participate in the synapses. This allows the brain cells to contact related cells that do not need to be localized in the same area of the brain. Effective contact is thought to be obtained through the connections made by neurons and neuroglia. This may give the actual associations a size big enough for protection against inactivation by the assumed specific natural clone inhibitors.

The contact between the cells in such associations reminds about the contact between melanocytes that are linked together by their offshoots. Therefore, the melanocytes seem to be protected against inactivation by the postulated natural clone inhibitor. Colored people do not lose their skin color when growing old. But the hair may nevertheless become grey, since the melanocytes in each hair root are unable to establish connections with melanocytes in neighbor hairs because the distance is too big. Therefore, the melanocytes of hairs form small separate communities. Each community comprises only of the relatively few melanocytes belonging to its own hair root.

The difference between working memory and long-term memory is explained in a way that harmonizes with what everyone has experienced; if something must be remembered the impression must either be strong or the topic that need to be remembered must be repeated actively and be associated and connected unto related topics.

Also immunological memory lasts differently. Some antibodies only last a few weeks, others for a few months. Antibodies may also last for the rest of the life.

Old or new experience and the presumed innate elements may be necessary for obtaining lasting memory. Since the brain has no specific immunologic organ, an infection of the brain has to induce production of antibodies within the blood/brain barrier. Therefore, it is believed that it is the bone marrow derived brain cells that produce the antibodies.

These cells must still have appropriate immunological capability that is necessary to form antibodies to the infecting agent. Since basic memory of the brain is believed to possess many characteristics such as the innate primed immune cells of the immune system, it may be natural that both memories are linked to the same type of cells. The other choice is the neurons. But they cannot divide and have never been reported showing many characteristics.

Then it is clear that the neuroglia cells of the brain must at least, be as important as the neurons.

The many characteristics of the neuroglia cells can be perceived as data in a database. The question is how they are linked together. It is assumed that the neurons help to obtain suitable contacts. However, if the neuroglia cells from the bone marrow become too old, they may even be replaced as already indicated.

There may be a difficulty: Identical cells that are sufficiently collocated locally cannot be inhibited by Invasivol or other specific clone inhibitors. For the memory of the brain, however, it seems necessary that only one part of those partaking associations needs to be identical. The other part of these associations may be different since everybody has experienced that a topic that should be remembered needs to be associated to topics that may even be completely different.
The identical parts of the greater associations are like the trunk of a tree, the parts that may be varying or dissimilar are like the branches.

HIV is an example of how the brain can become infected with a virus that causes dementia. But there is no evidence of HIV infection of neurons in the brain. This infection can be transmitted to the brain through monocytes and end in macrophages. Astrocytes and microglia can participate in the infection. It is possible that toxic factors may escape from infected cells and affect other cells of the brain.

Dr. Gwenn Garden (in News from the Center on Human Development and Disability at the University of Washington Health Sciences Center, Fall 2002 Vol 14, # 1) says that it is not found death of neurons in HIV dementia. However, there is great loss of synapses between neurons. But a loss of synapses will lead to fragmentation of associations and consequential memory loss.

Earlier the neuroglia cells were supposed to be supporters of the neurons. Now it is probable that they are important for the function of associations. They may be infected, can probably produce antibodies, be connected to neurons and other neuroglia thru synapses and be replaced.

Viral infection of some of these cells is believed to make them different from what they used to be and the cell mosaic increased accordingly. Then the assumed natural specific clone inhibitors could attack more efficiently.

The same mechanism makes the working memory more vulnerable than the greater associations of the longer lasting memory. These small associations with the fewest cells in contact with each other are close to the critically low number of cells required for being sufficiently remembered. HIV dementia is an example of viral cause of demetia.

But since it probably is cells from the blood, that carry the virus, maintain the infection and induces antibodies in the brain: it is possible that such cells can be replaced by the constant production of cells in the bone marrow. Then replacement of old cells by new ones from the bone marrow makes both immunological and brain memory resistant to the effect of the assumed specific clone inhibitors. Missing replacement, however, may affect memory seriously. 

Only some of the HIV-infected individuals get dementia. This complication will not improve in everyone after modern HIV therapy (HAART). As HIV can develop dementia, also TT virus that sometimes is found in the brain may be capable of attacking the brain similarly. Even though almost everyone is infected with TT virus, it is still not clear if and how the brain is affected.

 

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