Alzheimer disease and neurostimulation pacemaker

The powers of cognition (the ability to recognize people, places, things and relationships) are believed to take place in the frontal lobe areas of the brain. Some theorists believe that when certain areas of the frontal lobe degrade, so do the rapid access to the entire brain’s cognitive networks. New research seems to be emerging on creating digital pacemakers to stimulate those tissues of the frontal cerebral cortex that otherwise might develop Alzheimer Disease.

Cognition is about thinking and interpreting sensory perceptions – touch, see, hear, smell, and taste. We create emotional attachments to these senses and the viability of those senses off significant contributions to survival and growth. These begin at birth. Some say before birth, as evolutionary genetic markers pass along to generations.

Many people get frightened when they seem forgetful or get stuck on that tip-of-tongue phenomenon. Some fear these are signs of Alzheimer Disease. Other causes for memory problems can include aging, medical conditions, emotional problems, mild cognitive impairment, or another type of dementia.

Alzheimer Disease was once exclusively attributed to aging. It is the degradation of the ability to develop and access cognitive networks. Simply put, it isn’t. Many adults maintain cognition throughout their entire lifespans. Alzheimer disease may also form at much earlier ages. Cognition is a very lively, experimented topic. The development of Alzheimer disease and cognitive research are part of a mutually cohesive network with many branches. Can brain stimulation of certain areas improve chances of reducing or avoiding the effects of Alzheimer disease?

The use and research of brain pacemakers is less than a decade old and was originally developed to help treat Parkinson’s disease. A significant research sponsor is Michael J. Fox, a popular TV actor who was diagnosed with Parkinson’s.

When it comes to Alzheimer Disease, there are many memory disorders. Currently research theorists on the development of Alzheimer disease debate inferences of causality.

The problem has been that as it emerged beyond the aged norm of senility, Alzheimer’s disease was diagnosed with complete accuracy only after death, when microscopic examination of the brain reveals the characteristic plaques and tangles. This leads to questions as to why so many living people are being diagnosed with Alzheimer disease?

There has been much evidence that has shown how mice kept in a stimulated environment (vs mice in a non-stimulated environment) developed more brain tissue and neuron networks. Neurologists have been discussing that physical exercise produces BDNF or Brain-derived neurotrophic factors. BDNF, it is believed, promotes the survival of nerve cells (neurons) by playing a role in the growth, maturation (differentiation), and maintenance of these cells. It may play a role in building new neuron networks. Some studies support that BDNF increases as a result of physical exercise, aiding neuronal health. The presence of BDNF acts as a natural stimulant for certain brain areas. Since BDNF is genetic, can the reduction or absence of BDNF be behind some cognitive declines?

Cardio-exercise, REM Sleep, Antioxidants found in Coffee or Tea and Meditation help produce BDNF. Subsequently, stress, sugar, and social isolation may reduce BDNF. As such, some that are immobile or old (lacking social networks) might be developing some cognitive impairment because of lower BDNF levels.

According to BBC News,Doctors have known for some time that loneliness is bad for the mind. It leads to mental health problems like depression, stress, anxiety, and a lack of confidence. But there’s growing evidence that social isolation is connected with an increased risk of physical ill health as well. Again, stimulation helps cognitive wellness.

Use of brain pacemakers to help prevent cognitive decline is relatively new and few agree where they should be implanted. Nonetheless, Nanobioelectronics represents a rapidly developing field with broad-ranging opportunities in fundamental biological sciences, biotechnology, and medicine. Instead of referring to these as pacemakers, I prefer neuroprosthetics for monitoring and treating neurological diseases that may help resolve some of those cognitive pathologies that we only are beginning to fathom. Be it Parkinson’s, dementia (there are 4 types of dementia), aphasia, or Alzheimer disease symptoms, there are futures to behold.

There are many things that disrupt access to memories. Finding the seat to how memories are retrieved, processed and accessed is very complex and often to broad to even consider. Normal memory function involves many parts of the brain. Any disease or injury that affects the brain can interfere with memory. Amnesia, for example, might result from a physical trauma from an injury or accident. It may also develop from other causes, often undefined. Dissociative amnesia is organic and may results from a medical or psychological cause as opposed to direct damage to the brain.

There are two types of amnesia:

Anteror Grade Amnesia – Anterograde amnesia is a loss of the ability to create new memories after the event that caused the amnesia, leading to a partial or complete inability to recall the recent past, while long-term memories from before the event remains intact. In a sense, one with Anteror Grade amnesia has no short-term memory.

RetroGrade is a loss of memory-access to events that occurred, or information that was learned, before an injury or the onset of a disease. … It is not to be confused with antero-grade amnesia, which deals with the inability to form new memories following the onset of an injury or disease. One with retrograde may create new memories.

While neuroscience has made inroads at understanding the locations of where memories are stored and, possible treating amnesia. Yet, as result of research, amnesia – particularly antero-grade amnesia – was medically induced. This happened in the case of H.M.

The high incidences of cognitive loss and Alzheimer disease continue despite vast experimentation and research. Are more people being diagnosed with Alzheimer’s than before. There is a genetic marker, APOe-4, that seems to cite some evidence. Yet there are clean genes, dirty genes, and mutated genes. And nutritionists believe that this gene could be influence by dietary factors.

But is APOe-4 the only gene behind Alzheimer onset? Is there more research necessary? In the complex universe of the brain, there is obviously a vast network of questions covering nutrition, neurotransmitters, neurotransmission co factors, and infinite variables from environment and activity.

How would positive results of an APOe-4 test and scale influence one’s life, career, and state of living?

Are we dealing with Alzheimer disease, micro-stroke with cognitive decline, or other cognitive issues?

Of course many of the research experiments aren’t well funded. Perhaps some corporate donors might want to sponsor the research. Elon Musk, of Tesla and Space-X, is developing Neuralink that connects brains with computers. While Neuralink shows no ambitions to treat Parkinson or Alzheimer disease, it may stimulate other business leaders to consider possible investments.

I supported and studied frontal lobe dementia. Frontal lobe dementia does not cause memory loss, but it can exhibit cognitive and neurological problems similar to those caused by Alzheimer’s disease or stroke. The particular area of atrophy is not dissimilar between schizophrenia and dementia. Similar theorists believe that long-term memory storage may have been disaffected due to biochemical deficiencies in REM sleep. On either level, there are no clear etiologies that indicate or predetermine any causal effect of alzheimer disease type symptoms. Yet schizophrenic symptoms and dementia symptoms share some similarities that may be from a missing link between the cortex and the mid-brain memiry centers.

Genetics, diet, smoking, alcohol, substance abuse might be not highly associative to dementia. The problems involve neurotransmitters, catalysts, inhibitors, proteins, peptides, enzymes and a host of variability make us wonder ever more how this prefrontal lesion originated and its effects on memory and organized thinking.

A neurostimulation implant pacemaker therapy may be one significant approach to help suppress cognitive deficits. Using nano-electronic intervention for cognitive decline and avoiding Alzheimer disease, is a promising exploration into helping patients and families deal with cognitive decline. Whether a brain pacemaker will be a benefit is really up to further research as to where they could best stimulate possible reduction in Alzheimer disease decline. Yet, the pot of gold at the end of the rainbow may still require a series of quixotic games, puzzles, and questions to conclusively answer. We still don’t know what lies ahead. Do you?