AD Blog 1 of 6

By Terry Willard Clh, PhD

This material will be presented at the Kootenay Herb Conference on July 8^th, 2023 (https://herbconference.com/kootenay-herb-conference/).

We’ve all heard about, and know a bit about, Alzheimer’s and dementia. When some of us were growing up it was considered a rare occurrence. Well, now it is the third leading cause of death in North America—it is one of the fastest-growing serious health problems facing our world today. It has been estimated that by 2030, more than a third (some suggest more) of the world’s population over 60 years of age will be affected by this debilitating disease. Often called “the long good-bye,” this lingering disease is ruining many families. The effects of Alzheimer’s are far-reaching, and this insidious condition can take a heavy toll on individuals, families, and society as a whole.  

There are many things that can be done to greatly improve those odds, to decrease the chance of developing dementia and decrease the symptoms or severity of dementia. In this blog series, we are going to look at what we can start doing right now to produce better outcomes.

The brain is a complex organ, compartmentalized into different areas to ensure proper cognitive functioning—including motor skills, reasoning ability, emotional and sensory wellbeing, memory, and recognition. It also maintains the nervous system and hormonal balance and regulates other body functions.

Dementia is an umbrella term used to describe symptoms caused by neurological disorders that affect memory, thinking, behavior, and communication abilities. It is a degenerative disorder which results in the gradual decline of neural pathways and connections in the brain. Dementia primarily affects cognitive processes such as remembering, problem-solving, communication, orientation, and organization. The underlying cause of dementia can be attributed to a variety of factors including Alzheimer’s disease, stroke, head trauma, Huntington’s disease (HD) or Parkinson’s disease (PD). Symptoms vary from person to person but can include confusion, impaired judgment, disorientation, and difficulty carrying out everyday tasks. 

Early detection can help improve the quality of life for those affected. Treatment plans for those living with dementia vary depending on the type and causes of their condition; however, all treatment plans should be tailored to meet an individual’s needs and preferences.

TYPES OF DEMENTIA 

The four primary types of dementia are: 

1. Alzheimer’s disease (50–75% of cases of dementia)
2. Vascular dementia (20-30%)
3. Lewy body dementia (10-25%)
4. Frontotemporal dementia (10-15%)

Alzheimer’s Disease (AD)
Alzheimer’s disease (AD) is a progressively debilitating neurological (neurodegenerative) disorder that affects memory, cognition, personality, and eventually leads to death. It was first discovered by Dr. Alios Alzheimer in 1907 when examining the brain tissue from the autopsy of a woman with severe dementia at the age of 51. He noticed the deposition “of a peculiar substance in the cerebral cortex.” This substance has been found to be associated with the abnormal accumulation of amyloid beta-protein (Aβ) in the brain’s cerebral cortex. 

Beta-amyloids hinder neuron traffic by forming plaques between cells which results in cell death and eventual shrinkage of the brain itself, leading to further memory loss. Early-onset Alzheimer’s can be caused by genetic issues, while late onset can commonly be associated with other health conditions such as diabetes, hypertension, head injury, heart ailments, sedentary lifestyle habits, smoking, poor nutrition, obesity, or LDL (bad) to HDL (good) cholesterol ratios. 

By engaging in healthy lifestyle activities such as regular exercise, proper nutrition, and socialization, individuals can greatly reduce their risk factors for developing this disorder. 

Currently it is believed that there is no cure for dementia or Alzheimer’s Disease, but pharmaceutical medication can be prescribed that helps lessen its effects. We will look at allopathic, herbal, and nutritional methods to reduce and sometimes reverse Alzheimer’s symptoms. 

Alzheimer’s Disease Neuropathology

AD has distinctive neuropathologic features that include:^[1]

• Plaque formation
• Amyloid deposition
• Neurofibrillary tangles
• Granulovacuolar degeneration
• The massive loss of telencephalic neurons

AD is characterized by an array of cognitive and behavioral symptoms that are thought to be linked to abnormal changes in cholinergic neurotransmission. These changes are primarily caused by a decrease in the activity of the enzyme choline acetyltransferase (which is responsible for synthesizing the neurotransmitter acetylcholine) as well as impaired neuronal transfer of choline. 

The tendency to develop Alzheimer’s disease is multifactorial rather than exclusively genetic or infectious in origin: it appears to be a modern-day affliction caused by a combination of environmental, immunological, dietary, and genetic factors. Psychological issues including stress and other emotional factors appear to be associated as well. 

The primary clinical manifestations of Alzheimer’s include:

• Dementia as well as impairments in understanding language and other behavioral abnormalities. 
• Confusion, impaired memory recall, difficulty speaking, deficient judgment skills and abstract thinking abilities, 
• A sense of alienation from oneself, apathy towards once enjoyable pastimes and activities,
• Lack of creative expression, and reduced capacity for displaying affection. 

Language disturbances seen in Alzheimer’s patients can take the form of difficulty finding meaningful words during conversation or writing. AD patients often have difficulty performing everyday physical tasks like dialing phone numbers or unlocking doors. Other associated behaviors may include a deterioration in personal hygiene practices, wearing inappropriate clothing (e.g., not suitable for the weather or not matching the social situation, such as sweatpants to a formal dinner party), disruption in social etiquette, often misplacing items, regular traffic accidents, irritability, obstinacy, suspicion, short attention span, and being unable to comprehend basic instructions.^[2],[3],[4]

Etiology

As suggested above, the pathology of AD is characterized by the accumulation of amyloid-β (Aβ) proteins, which form into plaques between neurons, and the formation of neurofibrillary tangles caused by tau proteins. Over the past few decades there has been a tremendous amount of funding for and research into the root cause of AD. Most of this work has focused solely on amyloid beta-protein plaque formation as the cause of AD. Unfortunately, this has not produced therapeutic results that have been hoped for. Many researchers have started to think that the formation of neurofibrillary tangles associated with the tau proteins is the result of some other underlying pathology associated with AD and not the cause of it at all. There is no question that this plaque is associated with AD, being the star indication of its identification, but it is not THE critical causal factor of the underlying pathology. (And thus, targeting the plaque as a treatment for AD has not been resulting in the therapeutic outcomes, we were all searching for.) In fact, several experts now theorize that the plaque is the body’s (most likely the immune system’s) response to some toxins (most likely insulin) possibly threatening the mitochondria, thus the plaque may be trying to be a temporary solution, not the cause. 

Tau is a protein found in neurons, which are the cells that form our nervous system. Tau works by forming microtubules—tube-like structures that provide internal stability to nerve cells and ensure efficient transportation of proteins and other molecules throughout the neuron. In diseases like Alzheimer’s, however, tau proteins detach from the microtubules and join with other tau proteins inside the cell. This leads to an abnormal accumulation of tau proteins which results in the collapse of microtubules, forming structures called “tangles.” These tangles resemble a lump of dried out spaghetti, disrupt communication amongst neurons, and can cause them to malfunction and eventually die.^[5]

These pathology hallmarks are compounded by persistent abnormal glial cell activation which is indicative of neuroinflammation. Moreover, evidence is growing that aberrant immune system regulation may play a part in the development of AD as well. 

Genetic factors are estimated to play a major role in the development of AD, and changes in the relevant genes typically lead to symptoms developing before 50 years of age. Of particular relevance is the Apolipoprotein E (ApoE) gene found on chromosome 19: a variant of this gene, referred to as ApoE4, increases levels of ApoE proteins within the brain, which can cause an overabundance of Aβ proteins that can lead to AD pathology. It has been proposed that ApoE4 may also influence AD through other Aβ-independent pathways. In contrast, those who have an allele for the e2-type ApoE gene show significant protection from developing AD pathology. 

It is evident that AD is a multifactorial problem, being more of a constellation of concerns rather than simply one causative culprit. We are going to focus on several of these suspected contributing factors over the next few blogs. 

Some of these players in the AD story are:

1. Mitochondrial dysfunction
2. Traumatic injury
3. A diabetic glucose insulin issue
4. Environmental toxins
5. Dividing AD into subgroups to help with treatment

See you in Blog 2 of this series.

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^[1] Ballard C, Gauthier S, Corbett A, et al. Alzheimer’s disease. Lancet. 2011;377(9770) 1019–1013.

^[2] Rubin, E. ed. 2001. Essential Pathology. 3^rd ed. Philadelphia: J.B. Lippinocott.

^[3] Berkow, Robert ed. et al. 1992. The Merck Manual of Diagnosis and Therapy. 17^th ed. Rahway, NJ: Merck and Co.

^[4] Roberts, H.J. 1996. Allopathic Specific Condition Review: Alzheimer’s Disease. Protocol Journal of Botanical Medicine. 2(1): 94-106.

^[5] MAPT microtubule associated protein tau [ Homo sapiens (human)]; https://www.ncbi.nlm.nih.gov/gene/4137