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What is Alzheimer’s disease?

Alzheimer’s disease is a progressive neurodegenerative disorder that impairs memory, thinking, behaviour, and the ability to function independently. It reflects a gradual disruption of brain systems responsible for cognition (thinking, memory, and decision-making) and regulation.

Although symptoms most often appear later in life, underlying biological changes in the brain may develop decades before clinical signs become evident. Early stages commonly involve mild cognitive impairment (subtle but measurable decline in thinking ability), while more advanced stages may include significant memory loss, disorientation, language difficulties, impaired judgment, and reduced ability to perform everyday tasks.

Alzheimer’s disease is now understood as a multifactorial condition, arising from interacting metabolic, vascular, inflammatory, genetic, and lifestyle-related influences rather than a single isolated cause.

Medical standard of care

The standard medical approach to Alzheimer’s disease focuses on diagnosing cognitive decline and managing symptoms while attempting to slow progression where possible. Current treatments do not reverse the disease and place limited emphasis on nutritional, metabolic, or environmental contributors to brain degeneration.

Conventional treatment includes cognitive medications and supportive care aimed at maintaining daily function and safety. Lifestyle measures such as exercise and vascular risk management may be recommended but are generally considered supportive rather than primary treatment.

Medications commonly used for Alzheimer’s disease include:

  • Donepezil
  • Rivastigmine
  • Galantamine
  • Memantine

These medications act on brain signalling chemicals involved in memory and learning, particularly acetylcholine and glutamate. They may temporarily stabilize symptoms but do not stop disease progression.

Care typically also includes support for mood and behavioural changes, caregiver education, safety planning, and long-term care planning as the disease advances.

Why consider an orthomolecular approach?

Alzheimer’s disease can be caused by many different factors, as shown by both research and clinical experience. The medical standard of care addresses only some of these factors.

An orthomolecular approach:

  • identifies the drivers and causes of Alzheimer’s disease and focuses on addressing them
  • addresses the specific biological factors that may be affecting each individual
  • works WITH the body to restore balance and normal function, and considers the person with the condition versus just the condition
  • addresses nutrient depletions and other factors that promote Alzheimer’s disease
  • can be done SAFELY in conjunction with most medical interventions

Mechanisms of Alzheimer’s disease progression

1. Protein Misfolding and Impaired Clearance
Accumulation of damaged or misprocessed proteins

  • Amyloid and tau protein accumulation – Misfolded proteins aggregate into extracellular plaques and intracellular tangles that disrupt cellular structure and function.
  • Impaired proteostasis – Dysfunction of cellular “quality-control” systems impairs protein folding, repair, and degradation.
  • Reduced glymphatic clearance – Reduced cerebrospinal fluid–mediated waste clearance limits removal of metabolic byproducts, particularly during sleep.

Amyloid Precursor Protein (APP) is a normal brain cell protein that can be processed into either harmless fragments or amyloid-β, depending on how it is cut.

  • α-secretase pathway = “good”
    Produces non-harmful, often beneficial fragments
    → Increased by: healthy cellular conditions
  • β-secretase pathway = “bad”
    Produces amyloid-β (Aβ) (via β- and γ-secretase cleavage)
    → Increased by: aging, inflammation, oxidative stress

Tau stabilizes microtubules that transport materials inside neurons. When tau becomes hyperphosphorylated, it forms tangles and disrupts this transport system, leading to synaptic failure and cell death (Butler & Walker, 2021; Mold et al., 2021).

The glymphatic system is a brain-wide clearance pathway that uses cerebrospinal fluid to remove waste. Dysfunction of this system reduces clearance of amyloid and other toxins (Quevedo et al., 2023).

2. Metabolic and Energy Failure
Brain cells can’t produce enough energy

  • Brain insulin resistance – Brain cells don’t respond properly to insulin, making it harder for them to take in and use glucose (sugar). This reduces their ability to produce energy and contributes to a brain energy deficit
  • Mitochondrial dysfunction – Impaired mitochondrial activity reduces ATP (cellular energy) generation and increases production of reactive oxygen species (ROS), contributing to cellular stress.
  • Brain energy deficit – Neurons receive or utilize insufficient metabolic fuel (glucose and/or ketones) to function normally.
  • Oxidative stress – Excess reactive oxygen species overwhelm antioxidant defenses, damaging lipids, proteins, and nucleic acids.

3. Barrier and Vascular Dysfunction
Loss of protection and nourishment

  • Blood flow reduction – Reduced blood flow to the brain limits delivery of oxygen and nutrients required for neuronal maintenance and function.
  • Blood–brain barrier (BBB) breakdown – Increased permeability of the barrier allows circulating toxins, immune mediators, and inflammatory signals to enter brain tissue.
  • Optimize the amounts of nutrients that regulate homocysteine levels:
    • B-vitamins, especially vitamin B2, vitamin B6, folate, vitamin B12
    • methyl donor molecules: choline, betaine, SAMe
    • minerals: zinc, magnesium
  • Increase intake of leafy greens, legumes, and vegetables, eggs, fish, and meat.
  • Reduce alcohol and coffee intake (if excessive).

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