Alzheimer’s disease (AD) is a heartbreaking condition where an individual plunges ever deeper into a state of dementia, losing cognitive function, memories and essentially who they are as a person. Alzheimer’s is the most common neurodegenerative disease. However, new research shows that different treatment approaches may provide a breakthrough in combating the slow mental deterioration of Alzheimer’s.
Alzheimer’s and Brain Function
To understand how various chemical and structural changes in the brain can lead to the formation of Alzheimer’s disease, we first need to understand how the brain works. The brain is like a maze of subway tunnels and trains, each with a specific destination. The “tunnels” are called neurons (brain cells). In these tunnels riding the “trains” are “people” called neurotransmitters (brain chemicals). Each neurotransmitter has a specific job to do, and if the “trains/tunnels” (neurons) are running late or stopped completely, the neurotransmitters can’t go to work. When neurotransmitters can’t get to their job, bodily functions can’t happen.
Underlying Causes of Alzheimer’s Disease
A chemical compound in the brain known as an amyloid (protein fragments) is a common byproduct of cellular division. However, there are two types of amyloid fragments (Aß40 and Aß42), one good, and the other no so good. Aß40 can be broken down and eliminated from the brain and the body, however, Aß42—in an unhealthy brain—cannot. Aß42 forms molecular mounds, these mounds build up over time and form plaque. This amyloid plaque then blocks the natural pathway for neurons and neurotransmitters.
Think of it this way, if you were to stop taking the garbage out, it’d start piling up in your house. Over time, the accumulated garbage would block hallways, making moving from room-to-room very difficult. This is the same situation neurotransmitters are facing in the brain—they are blocked by molecular garbage known as amyloid plaque. When this happens, calcium levels can become unbalanced (a necessary component for brain function), neurons stop delivering neurotransmitters to perform their job and, as a result, cognitive function (thinking) deteriorates.
Another negative product of bad amyloid buildup is something called Tau hyperphosphorylation. Think of Tau as the people who maintain the neuron tunnels, without them, the tunnels collapse or become tangled together. Hyperphosphorylation makes Tau “stick together.” Think of a bunch of construction workers talking instead of working. When Tau can’t maintain the neuron tunnels/trains because they are too busy talking, the entire “subway system” (the brain) shuts down, neurons are stranded, and the resulting effect is dementia and Alzheimer’s.
Oxidative Stress and Age
Oxidative stress is a condition where the body produces or consumes free radicals, which then overwhelm various bodily systems causing illness, disease, even cancer. Free-radicals are chemical compounds with an unpaired electron that can pull electrons away from other chemical compounds in the body, causing major issues. Think of free radicals then as chemical level muggers, stealing electrons away from others. One of the issues associated with Alzheimer’s disease is an abundance of free radicals. These gangs of free radicals destroy neurons. To make matters worse, chemical “security guards” (antioxidants like GSH) which protect the neuron tunnels and keep rebellious free radicals at bay, are often found missing (or present but at greatly reduced levels) in those with Alzheimer’s disease.
Free radicals can also be caused when advancing age and vascular risk factors combine—which can cause a condition known as “attained threshold of cerebral hypoperfusion” (CATCH). This condition causes the deterioration of capillaries supplied to the brain. When this happens, it puts stress on other cells, and those cells expend energy of which free radicals are an unfortunate byproduct. Free radicals can wreak havoc on neurons.
High Cholesterol and Alzheimer’s Disease
High cholesterol has been linked to the formation and delay of Alzheimer’s. In general, and sticking with our metaphor, cholesterol (good cholesterol) tends to act as the garbage man. A specific cholesterol known as Apolipoprotein (Apo) helps the brain and body get rid of that annoying amyloid garbage laying around.
Can Alzheimer’s Disease make Sugar Less Sweet?
No. However, insulin may play a role in the formation of Alzheimer’s, more specifically the accumulation of amyloid plaque. Insulin receptors are very sensitive when they are activated for prolonged periods they become less reactive. Insulin helps remove amyloid plaque like Apolipoprotein by “taking it out to the street” where Apo can pick it up.
However, when there is a lot of amyloid garbage, insulin can become “stressed out” and stop taking the garbage out altogether. This means that more Aß42 garbage sits in the neuron tunnels, blocking neurotransmitter commutes, jumpstarting Alzheimer’s and related dementia.
Neurotransmitter’s role in Alzheimer’s Disease
Acetylcholine is a major neurotransmitter responsible for maintaining/producing other chemicals that can help control inflammation of cells within the brain. These cholinergic neurotransmitters are also responsible for one of the ways the commonly used drug Nicotine interacts with the brain. A specific nicotine receptor (nAChR) can increase Tau phosphorylation, which as you remember from before, is like having the workers responsible for maintaining the neuron “subway tunnels” on break. Ironically, Nicotine comes from smoking, so think of acetylcholine and Nicotine’s effect on the brain as making Tau take a long smoke break, leaving the neurons to deteriorate.
Glutamate is another neurotransmitter that may be closely tied to the formation of Alzheimer’s. If glutamate gathers outside of neurons (glutamatergic excitotoxicity), getting into the “subway tunnel” for neurons to get to work may become hard. As a result, neurotransmitters have to use other doors to get in, this also lets calcium ions into the neuron (Ca+2). Large amounts of calcium ions within the “subway system” can cause it to gradually shut down over time.
What does this mean for Alzheimer’s?
By focusing on the underlying causes of Alzheimer’s disease, new medications can be created, and existing medications can be used in new ways. The goal is to target amyloid plaque, Tau hyperphosphorylation, Cholesterol, insulin receptor sensitivity, and control the abundance of specific neurotransmitters (like SSRI’s and MAOI’s do for depression).
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