Alzheimer's Disease Treatment Program

Alzheimer’s disease (AD) often starts as memory-related issues and is associated with mild cognitive impairment. There are different stages of Alzheimer’s disease, and the earlier in this process you present to our office, the better chance we have of helping your symptoms.

Alzheimer’s disease is a form of dementia affecting the areas of the brain that control your thinking, memory, and reasoning. Cognitive decline and memory loss are among the first symptoms associated with AD. Initially, these symptoms don’t interfere with someone’s ability to live a “normal” life, but as the disease process continues you develop mild cognitive impairment, and continue to decline. Alzheimer’s has been said to be irreversible, however, reducing and supporting the risk factors that contribute to developing MCI and Alzheimer’s may help slow the degeneration of neurons.

Alzheimer’s affects the frontal and temporal lobes which are both involved in short-term memory, working memory, reasoning, and executive functions. Unfortunately, early on in disease development, you may not realize these things are happening. Initially your friends and family may recognize that your memory is worsening, and the ability to reason or make good decisions is beginning to decline. This can progress as the chart below indicates.

As the areas of the brain degenerate the neurons are dying off. This creates a loss of volume in the physical brain. Below is an image comparing a normal brain and a brain of someone with Alzheimer’s disease.

Amyloid-Beta and Tau Proteins – Signaling Between Neurons

Think of a neuron-like a superhighway, with a frontage road running parallel between neurons. Tau proteins are found inside the neuron on the “superhighway” and are responsible for intracellular transmission (volume of information) while Amyloid Beta peptides are found between neurons (on the frontage roads) and are responsible for extracellular transmission (speed of information) and work together with the brain’s immune system cells called glial cells.

Breakdown in Intracellular and Extracellular Signaling

Multiple factors such as genetics, brain injury, inflammation, thyroid dysfunction, insulin resistance, and chronic infections (viruses, mold, bacteria, parasites) can all impact the development of amyloid-beta and tau proteins that can cause misfolding, neurofibrillary tangles, amyloid-beta plaquing.

When the above factors are present, breakdown occurs in the building of Tau and Amyloid Beta. Both Tau proteins and Amyloid Beta begin building abnormal proteins which result in Tau protein misfolding and neurofibrillary tangles that create a massive traffic jam on the superhighway inside the neuron. At the same time, Amyloid-Beta plaques are formed by basically gluing the brain’s glial cells and nerve debris together to the outside of the cell causing a slowing of signaling.

These processes are both associated with neurodegenerative disease, Tau proteins have been associated with Parkinson’s Disease and amyloid-beta plaques have been associated with Alzheimer’s Disease.

Causes of Alzheimer’s are still being discovered and researched, but there are a few commonalities in the development of AD. (read more)

• Genetics- APOE genes may indicate an increased risk for developing Alzheimer’s- they’re described as APOE E2, E3, and E4.
  • APOE2 indicates a lower risk
  • APOE3 indicates a normal risk
  • APOE4 indicates an increased risk

Now, test results for an APOE2 don’t mean you can’t or won’t get Alzheimer’s, and a positive test for APOE4 doesn’t mean you definitely will develop Alzheimer’s, it is just one of the most commonly discussed risk factors to consider when addressing lifestyle and nutritional modifications when supporting brain health, or directing care towards mild cognitive impairment and the diagnosis of alzheimer’s.

“The APOE4 gene essentially over-competes against E2 and E3 for the insulin receptor and goes on to create more damage inside the neuron by clumping together and creating toxic end products” — Mayo Clinic (Read More)

Blood sugar dysregulation (aka insulin resistance, aka Type-3 Diabetes which occurs in the brain) is a major, if not the biggest contributor to the development of Alzheimer’s. With all the risk factors we list, blood sugar imbalances seem to be the biggest trigger for tipping the scales towards degeneration of these parts of the brain.

“Type 3 diabetes occurs when neurons in the brain become unable to respond to insulin, which is essential for basic tasks, including memory and learning. Some researchers believe insulin deficiency is central to the cognitive decline of Alzheimer’s disease.” — Mayo Clinic (Read More)

Inflammation is another big contribution, particularly mid to later in life. Inflammation is the response of the immune system to an intruder or something that isn’t supposed to be in the body. The brain is protected only by a single layer blood-brain-barrier (BBB) and when inflammation causes this to open, the brain becomes inflamed, and it continually turns on the immune system (aka microglial or glial cells). Once the glial cells are active it is difficult to turn them off, however, certain types of herbs, nutrients, and supplements have been shown to help downregulate some of this brain-based immune inflammation.

“Over the last decade, the presence of a sustained immune response in the brain has emerged as a third core pathology in AD. The sustained activation of the brain’s resident macrophages (microglia) and other immune cells has been demonstrated to exacerbate both amyloid and tau pathology and may serve as a link in the pathogenesis of the disorder.” — Alzheimer’s & Dementia : Translational Research & Clinical Interventions (Read More)

Chronic Traumatic Encephalopathy, history of concussion, and other head injuries are large contributors to brain inflammation as they also activate the glial cells as indicated above.

“Like Alzheimer’s dementia, CTE is characterized by tangles of an abnormal form of the protein tau in the brain. Unlike Alzheimer’s dementia, these tangles typically appear around small blood vessels, and beta-amyloid plaques are only present in certain circumstances.” — Alz.org (Read more)

Our approach to working with Mild Cognitive Impairment and Alzheimer’s/Dementia patients targets the underlying pathophysiology and risk factors noted above. We run labs to establish genetic risk factors, assess blood sugar stability, evaluate inflammation levels, history of TBI or concussion, and continue diving deeper to look into gut health, stress management, and nutrition/supplementation to help alleviate the burden of these underlying risk factors.

Call today to see if Arizona Chiropractic Neurology and Brain Center can help you.