Neurodegenerative diseases (NDDs) are a spectrum of disorders that attack brain and nervous tissue, interfering with coordinated muscle control and/or the ability to learn, think clearly, manage our emotions, or to access our memories. [1]

This group of neurologic disorders includes the

demyelinating disorders   [2] like Multiple Sclerosis,
movement and cerebellar disorders     [3]   like Parkinson's disease,
and the dementias,     [4]   which mostly includes Alzheimer's disease.

Their incidence rates in America are:

    Multiple Sclerosis      947,000  [5]
    Parkinson's Disease   1,200,000  [6]
    Alzheimer's Disease   5,800,000  [7]

Although each one of these diseases target different portions of the brain, there are numerous similarities in the decline of those tissues, and in how they begin to form fatty-protein tangles which interrupt nerve function.

Our first (2008) review of NDDs [8 A] discussed a meta-analysis [8 B] of 59 different randomized clinical trials that assessed the five FDA-approved drugs for treating Alzheimer's. That study revealed that all five drugs currently in use to manage Alzheimer's all failed to provide “clinically important improvements” for the patients who took them. [9]

The reviewers also advised that: “Clinicians must take into account the adverse effects of these drugs, and balance that potential harm against the modest potential benefits.” [9]

The five approved medications include the cholinesterase inhibitors donepezil, galantamine, rivastigmine, tacrine and the neuropeptide-modifying agent memantine. Since 2013 several other Phase II drug trials have also failed to provide any measurable benefits.

Our second (2013) newsletter [10 A] provided an updated overview of Alzheimer’s (AD), reviewing the dramatic impact that the pharmaceutical industry has on the direction of research, and also examined the evolving theory that insulin insensitivity appear to be a major contributor to AD development, leading some researchers to now refer to AD as “Type 3 diabetes”.   [10 B]

The Chicken or the Egg?

When someone dies of a neurodegenerative disease like Parkinson’s or Alzheimer’s, it is possible, with modern technology, to study their brain tissue, [11] and to run extensive lab analyses, to determine how those diseased cells differ from “normal” brain tissue. [12], [13]

Those observations have revealed that:

• Dramatic changes occur in cellular architecture:   These include damage to, or even complete disintegration of the microtubules [14] that control intracellular transportation, provide general structural support, and choreograph cell division.

• Extensive disruption of cellular energy production:   Mitochondrial dysfunction and damage reduces cell function while also increasing oxidative damage, causing a vicious and self-perpetuating cycle of damage that ultimately leads to neuron death.   [15]

• Lower nutrient levels in damaged brains:   Deficiencies of antioxidants, trace minerals, flavonoids, vitamins, and omega-3 fatty acids are commonly found in damaged brain tissues.   [16],     [17]

• Proliferation of bizarre proteins and modified fatty acids:   Chief among these are amyloid plaques and advanced glycation end products (aka AGE proteins) that disrupt nerve transmission.   [4],     [18]