Ketamine and Alzheimer’s Disease


“Alzheimer’s disease is a progressive neurodegenerative disease characterized by insidious cognitive decline and loss of memory function.” This was how Alois Alzheimer, a German neuropathologist, first described the disease in 1906. It is well known around the world for the heartbreaking conditions it forces its 35 million victims—and their loved ones—to suffer from. It forces children to be parents—for their parents.

It removes all traces of identity and erases all memory and dignity. Alzheimer’s disease slowly robs its victims of themselves, taking everything, and leaving nothing but an empty shell…a shell that gets lost in their own room, forgets their own name, who they are married to, who their children are, and eventually how to eat, clean, and speak.

In the United States alone, Alzheimer’s disease affects 5.5 million people, with that number expected to quadruple by 2050, when the disease is estimated to affect over 22 million people. It is one of the only causes of death that has increased by more than 66% over the last decade. And, despite many advancements in medicine, there are still no drugs to treat it.

According to a medical paper published in 2004, by The University of California’s Department of Medicine, memory loss “correlates better with synapse loss than with plaques or tangles.” It describes how specific dysfunction in the neurons could contribute to cognitive failure in Alzheimer’s disease. This is due to a large loss of drebin, a protein found in neurons and connected to cognitive function. It explains that these synapses are vulnerable to aging and oxidative stress from high dendritic energy consumption.

While there are no official treatments for Alzheimer’s disease yet, there may be options available as a preventative measure for those who are predisposed.

There has been research on the effects of sub-anesthetic doses of ketamine. One study published in 2018, by the Department of Anesthesiology in Hebei, China, explains that ketamine decreases the density and length of dendritic spines. In that same year, the Department of Automation in Shanghai, China, published a paper on dendritic integration in pyramidal neurons.

That paper explains that an excessive number of active synapses over a period of time could increase the energy burden. Perhaps then, through the use of ketamine, the growth of fewer, newer, and leaner spines could be promoted to replace the older, denser ones. This could aid in the prevention of developing memory loss from a disease like Alzheimer’s due to a reduction in metabolic energy consumption, their relocation, and capacity on the synapse.

Since ketamine affects memory formation and learning in the brain, it has a number of therapeutic uses. Traditionally, it has been used as an anesthetic. However, more recently, in smaller doses, it has grown in popularity as a treatment for a number of conditions like depression, PTSD, pain, bipolar disorder, and other psychiatric conditions. Ketamine for Alzheimer’s is still very much in its infancy, though, so more research needs to be conducted to determine its full therapeutic purpose.

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