A Review of “Study Gives New Clues on How Alzheimer Spreads

by María Santiago-Valentín

 

The report presents the results of a research about how Alzheimer spreads in the brain. Alzheimer or dementia is a mental disease where the neurons progressively die. It was not certain before the order or process in which the cells infected each other.  Scientists and experts thought that the disease appears in certain areas in ways very hard to predict over a period of time. Other experts thought that there might have a predictable pattern in the dissemination of the disease in the brain, and the research results validate their thoughts with strong evidence.

According to the results of the research, the experts concluded that the Alzheimer disease seems to spread in a pattern that can be followed, where one neuron infects the neuron next to itself in the synapse region. The infected neuron releases the infection through the neurotransmitters in the axon that the dendrite of a healthy neuron will receive in the dendrites. The article is very optimistic because this revelation can help scientists find a way to halt the progression of the disease.

The researchers of this study used mice, and the mice were created to have deposits of tau, which a protein located in the long axons of the neurons. It is normal to see this protein located in the axon, but when tau abnormally locates or deposits itself in the cell by entering through the dendrites it is when the destruction and degenerative process of the neurons begins in the brain. The scientists followed the development of the tau in the brain of a mice for a one year and ten months. While mice aged the researchers observed how abnormal tau moved from the ethorthinal cortex which is the focal point of memory and where Alzheimer begins (location is in the temporal lobe) to the hippocampus (located in the center of the limbic system), and later onto the neocortex (located in the frontal lobe) which are the areas of the brain responsible to create and reserve the memories. The team observed that the infection or the progression of the abnormal tau happened in the synapse. That infection impedes the communication from one cell to the other one. The findings in the areas of the memory of the brain can help have an early diagnose of the disease and as early as it can be detected the better to either slow down or stop its progression. Current medication has overlooked the role tau plays in the spread of the disease since it has mainly focused on targeting the amyloid plaques which are the amino acid deposits found in brain patients with Alzheimer’s disease.

Second, for the scientific community the results of this research validate the thoughts that many experts share about a predictable pattern of Alzheimer disease. The predictable the pattern, the more accurate the diagnosis is, and more appropriate the treatment of the disease will be. Prevention is not an option at this point because scientists are aware that the abnormal presence of the tau is what spreads the disease, but what really triggers the beginning of the presence of the abnormal protein is not investigated in this particular research.

New medication needs to be developed to target the spread of the abnormal tau protein, in ways to slow down its generative effects or to really halt its dissemination in the synapse. The suggestion of new brain images for the early detection of the disease seems to be one of the approaches the neuropsychology community is going to follow (2012). The scientists are already detecting Alzheimer at its beginnings in the ethorthinal cortex and if a brain image shows the neuron infection spreading from the ethorthinal cortex to the hippocampus, the treatment can be improved by targeting the infected area to stop the disease propagation to the hippocampus and from there where memories are affected in the neocortex area located in the frontal lobe.

Medication that treats both chemicals tau and the amino acid beta amyloid is at this moment the approach the scientists will use to continue the treatment of Alzheimer.  The disease prevention should be the next prioritized area that the scientific community should focus. The researchers should look into common symptoms in patients before early stage like a minor ailment, mineral or vitamin deficiency that will trigger the disease.

In the field of education this research offers hope and new information about the dissemination of the disease to health care professionals, staff that deals with patients with Alzheimer, caregivers, the family of the patient, and the patient himself/ herself who suffers from the disease. These results bring new light and all human resources involved need to be aware of the efforts to halt or slow down Alzheimer. It usually appears after the person is 65 years old and it is crucial to detect early signs of memory loss in current information, change in behavior patterns and loss of memory of activities that routinely are performed automatically. These early signs seen in a loved one should prompt us to take her/his for a diagnosis. But if the disease unfortunately started, its progression depends on the immediate intervention of the patient’s caregivers to stop its dissemination. We also need to be well informed with updated information to dispel fallacies regarding causes and treatment. In our classrooms we need to help disseminate the new knowledge to our students, friends, and relatives when they are suffering the stress of having a loved one with this disease. This disease affects more than 5 million Americans according to the study.

It seems that the most logical and effective approach for the treatment of Alzheimer should be to target tau, but it is also important to follow current approaches for its treatment. The imminent degeneration of an infected cell that infect others, leaves room for the health care professional or family member to help the patient develop and use other areas of the brain that are not yet infected with memory games, trivia, repetition of events, seeing family pictures, asking her/him to retell what was read at a later time to exercise their short and long term memory. It is important to help the patient’s brain create new connections and start new rewiring of cells once his/her neurons begin to get infected.  It is very probable that is an area is affected another area that has not been affected yet will take over and the communication between the neurons that create the nervous impulses will not be blocked.

Now the areas for future research should focus on medication since no drug despite the $170 million dollars annually spent for Alzheimer treatment is able to prevent its spread. Researchers should find the chemical combination that can prevent, melt away, destroy, or block the degenerative effect of the abnormal form of the tau protein in the neurons. The medicine needs to go to the synapse region where the tau protein of an infected neuron is released by the axon before it enters into dendrites of a new neuron to infect and kill it.

 

Khan, Usman & Liu, Li & Provenzano, Frank & Berman, Diego & P Profaci, Caterina & Sloan, Richard & Mayeux, Richard & Duff, Karen & A Small, Scott. (2013). Molecular drivers and cortical spread of lateral entorhinal cortex dysfunction in preclinical Alzheimer’s Disease. Nature neuroscience. 17. 10.1038/nn.3606.

 


Published by Maria Santiago- Valentín