Reimagining Alzheimer's and Dementias: Outside the Box Cures and Treatments

When most people think about Alzheimer’s and dementias, their mindset tends to gravitate towards treatments rather than cures. Most believe that addressing symptoms is essential, but curing the disease remains an elusive goal. However, a novel hypothesis proposes a path outside the conventional medical box, suggesting a link between atherosclerosis and the development of Alzheimer’s disease. This article delves into this hypothesis and explores the potential for cures and preventive measures.

Defining the Disease

First, it is important to understand that dementia can have various causes, some of which can be addressed and potentially cured. For instance, poisoning, malnutrition, severe physical, emotional, or social stress can all contribute to the onset of dementia. When these underlying causes are successfully addressed, the disease can be cured. Similarly, if the cause is partially addressed, a partial cure may be achieved.

However, when it comes to Alzheimer's disease, defining a cure has proven challenging, mainly due to the lack of clarity in what constitutes a cure for a non-infectious disease. While it is relatively straightforward to define what a cure entails, the lack of interest in such a definition has hindered progress in finding cures. Our understanding of Alzheimer's primarily revolves around treatments, leaving us unsure if these treatments are moving us towards a cure or further away from it.

A Novel Hypothesis: Alzheimer's and Atherosclerosis

The novel hypothesis proposed here is particularly innovative and outside the traditional medical framework. It suggests that the release of catecholamines, such as norepinephrine and epinephrine, in the brain and bloodstream could be the underlying cause of Alzheimer's disease.

According to this hypothesis, norepinephrine released in the brain cortex breaks down elastic polypeptide chains and disulfide homocysteine "bridges" in the arteries. This process leads to a gradual build-up of atherosclerosis, which restricts blood flow to the brain, causing the brain to shrink and resulting in Alzheimer's symptoms. The beta amyloid deposits found in Alzheimer's brains are remnants of cleaved polypeptide chains from the damaged arteries.

Several factors can accelerate the release of norepinephrine and epinephrine, increasing the risk of developing Alzheimer's disease. These factors include mental, physical, and chemical stress, an unhealthy lifestyle, and a metabolic magnesium deficiency. Examples of chemical stress include smoking, alcohol consumption, caffeine, salt intake, and exposure to herbicides and pesticides.

The Role of Cerebrospinal Fluid (CSF)

Cerebrospinal fluid (CSF) plays a crucial role in maintaining the health of the brain. It is pumped through aquaporins wrapped around the arteries in the brain. The pulsating action of healthy arteries provides the mechanism for CSF to circulate through the brain. However, as atherosclerosis develops, the pulsation of the arteries diminishes, reducing the CSF's pumping action and leading to impaired circulation.

The build-up of beta amyloid deposits in the brain further obstructs the circulation of CSF, causing an overall impairment. It is hypothesized that a reduced circulation of CSF due to atherosclerosis could be a precursor to the buildup of beta amyloid deposits, as a healthy circulation of CSF could help wash away amyloid material as it is being produced.

The Seizure Hypothesis

Neurons in the brain emit a K ion during the start of each activity cycle, which creates an internal negative electrical charge. During recovery from activation, if a neuron retains its negative charge and captures a nearby K ion, it can lead to an excitotoxic seizure and destruction of the neuron. In healthy brains, the circulation of CSF helps to minimize the probability of K ion capture, but in areas with impaired CSF circulation, this probability increases exponentially.

The destruction of neurons due to an impaired circulation of CSF is proposed as the direct cause of Alzheimer's disease. The tau tangles that form in Alzheimer's brains are remnants of the destroyed neurons. Brain plasticity is capable of repairing and bypassing these destroyed neurons, but widespread damage and neuron destruction become evident only after extensive vascular damage has occurred, making a cure physically impossible at that stage.

Preventive Measures and Prophylactic Therapy

To reduce the incidence of early-onset Alzheimer's disease, a comprehensive healthy living program and prophylactic therapy should be adopted, ideally starting from an early age, preferably before age 30. This program should include a combination of lifestyle changes, dietary adjustments, and daily supplements. A few potential components include:

Healthy Lifestyle: Engaging in regular physical activity, managing stress, and maintaining a healthy diet can help reduce the risk of Alzheimer's disease. Supplements: Magnesium-L-threonate, vitamins D, B6, B12, and folic acid can help in managing the release of norepinephrine and epinephrine, thereby slowing down the buildup of atherosclerosis. Medication: Alpha and beta blockers may be considered to restrict the release of norepinephrine and epinephrine.

Such a comprehensive healthy living program and prophylactic therapy could not only reduce the incidence of early-onset Alzheimer's but also potentially play a role in lowering the risk of type 2 diabetes and vascular diseases.

In conclusion, this novel hypothesis provides a fresh perspective on Alzheimer's and dementias, emphasizing the potential for cures rather than just treatments. By understanding the underlying mechanisms of the disease, we can develop more effective preventive measures and treatments that could ultimately lead to a cure for Alzheimer's and dementias.