Alzheimer’s is a progressive neurodegenerative disease, and seeing a loved one gradually lose control over his life and relationships, fail to recognize you, and become dependent on others just to carry out simple daily tasks is very painful. Alzheimer’s disease-associated dementia is so common that it has come to be viewed as a normal consequence of aging. Fortunately, it is not.
In attempts to decode the secrets of memory, scientists have debunked several misconceptions regarding how we remember and why we forget. Previously, it was believed that memories are stored in the synapses that forge connections between brain cells and facilitate the transfer of signals. So it was believed that Alzheimer’s patients suffer from memory loss because their brain cells are damaged by the disease.
Scientists have now discovered that Alzheimer’s disease is actually caused by degeneration of neural networks or synaptic connections when the brain chemistry goes awry. According to them, the memories are in the molecular changes that take place within the brain cells themselves, rather than in synapses.
How do we remember?
The key to finding a remedy to reverse memory loss in Alzheimer’s disease patients lies in decoding how the memory, long-term memory in particular, works and why people forget. Long-term memory takes time to consolidate and is more stable than short-term memory. It is the basis of learning new skills and applying this knowledge to carry out various tasks. So scientists have tried to learn about the nature of long-term memory and how it is more durable in some persons than others to understand why we forget what we have learned or fail to learn at all because we cannot remember. These answers hold the clue to finding a way to reverse memory loss.
A recent study on humble sea snails (Aplysia) indicates that long-term memory is stored not in the synapses but in the bodies of neurons while synapses are needed for retrieving the memory. Damage to synaptic connections can be leading to the loss of memory since the memories cannot be retrieved from the neurons anymore. But preliminary research shows that the nervous system can also regenerate these synaptic connections and bring back lost memories.
The role of serotonin in forming long-term memory
For quite some time, neuroscientists had been pondering over the role of serotonin in aiding memory formation. According to a study on the fruit flies Drosophila, triggering their neurons to produce more serotonin facilitated learning by aiding memory creation.
A recent study confirmed the above findings. In the laboratory, Aplysia snails were subjected to mild electric shocks. The scientists discovered that when they gave the shocks, serotonin was released in the central nervous system of the snails. This led to the formation of synaptic connections that create long-term memories. During this process, the brain also produced new proteins that the scientists believe aided the growth of long-term memory. The connections stayed for a couple of days, which means that the “memory” of the electric shocks remained with the snails for some days after the experience.
These are, no doubt, interesting insights into the workings of the memory, but what the scientists discovered next was more encouraging. They segregated neurons from the snails in a Petri dish and added serotonin to these. New synaptic connections formed between the neurons. The scientists also discovered that the growth of new neural connections stopped if they added a protein synthesis inhibitor immediately after adding serotonin. Incidentally, protein synthesis is essential for memory formation and to preserve the functionality of neurons.
The above findings lend hope that scientists will soon discover drugs that can alter the brain chemistry and trigger new synaptic connections in Alzheimer’s patients who have suffered neural damage. This has a potential of restoring the lost memories.
But is there a way to prevent synaptic damage in the first place?
The role of amyloid-ß in causing synaptic dysfunction in Alzheimer’s disease
Researchers believe that synaptic failure in Alzheimer’s patients is associated with an excess of amyloid-ß (Aß) peptide in the brain. Certain types of the amyloid-ß protein lead to the formation of fibrils or plaques in the brain, and these deposits cause synaptic dysfunction. Moreover, certain forms of the amyloid-ß protein or Aß-derived oligomers negatively affect the structure and composition of synapses and trigger neural degeneration.
Aß peptides are abundant in the brain of patients with Alzheimer’s disease. The accumulation of Aß has also been associated with oxidative damage in the brain that disrupts the normal functionality of neurons. So it is evident that therapeutic methods that can prevent the proliferation of Aß peptides in the brain or inhibit their effects can go a long way in preventing and reversing memory loss in Alzheimer’s patients.
The human brain has the remarkable ability to remodel itself. It has been established that synaptic regeneration is one of the ways in which the brain remains flexible and aids in memory formation. These findings present a sliver of hope to patients and caregivers and spur scientists to explore therapies that can genetically alter brain chemistry and reverse neural degeneration. And it is not only Alzheimer’s patients who can look forward to a future of hope. People who are suffering from memory impairment caused by physical brain injuries or other neurodegenerative diseases can also benefit from these future therapies.
References
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Chen, S., Cai, D., Pearce, K., Sun, P., Roberts, A., & Glanzman, D. (2014). Reinstatement of long-term memory following erasure of its behavioral and synaptic expression in eLife, 3 DOI: 10.7554/eLife.03896
Crimins, J., Pooler, A., Polydoro, M., Luebke, J., & Spires-Jones, T. (2013). The intersection of amyloid beta and tau in glutamatergic synaptic dysfunction and collapse in Alzheimer’s disease Ageing Research Reviews, 12 (3), 757-763 DOI: 10.1016/j.arr.2013.03.002
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Lacor, P., Buniel, M., Furlow, P., Sanz Clemente, A., Velasco, P., Wood, M., Viola, K., & Klein, W. (2007). A Oligomer-Induced Aberrations in Synapse Composition, Shape, and Density Provide a Molecular Basis for Loss of Connectivity in Alzheimer’s Disease Journal of Neuroscience, 27 (4), 796-807 DOI: 10.1523/JNEUROSCI.3501-06.2007
Mucke, L., & Selkoe, D. (2012). Neurotoxicity of Amyloid -Protein: Synaptic and Network Dysfunction Cold Spring Harbor Perspectives in Medicine, 2 (7) DOI: 10.1101/cshperspect.a006338
Palop, J., & Mucke, L. (2010). Amyloid-?–induced neuronal dysfunction in Alzheimer’s disease: from synapses toward neural networks Nature Neuroscience, 13 (7), 812-818 DOI: 10.1038/nn.2583
Reddy, P., & Beal, M. (2008). Amyloid beta, mitochondrial dysfunction and synaptic damage: implications for cognitive decline in aging and Alzheimer’s disease Trends in Molecular Medicine, 14 (2), 45-53 DOI: 10.1016/j.molmed.2007.12.002
Sitaraman, D., Zars, M., LaFerriere, H., Chen, Y., Sable-Smith, A., Kitamoto, T., Rottinghaus, G., & Zars, T. (2008). Serotonin is necessary for place memory in Drosophila Proceedings of the National Academy of Sciences, 105 (14), 5579-5584 DOI: 10.1073/pnas.0710168105
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