ALZHEIMER'S DISEASE

 

• Alzheimer’s Disease afflicts 3% of persons aged 65 to 74.
• Alzheimer's Disease afflicts 18.7% of persons aged 75 to 84.
• Alzheimer's Disease afflicts 47.2% of persons aged 85 and over.
• Alzheimer’s Disease is more prevalent in females than in males.
  
  There is a genetic predisposition to being afflicted - the likelihood of a close relative of an Alzheimer's Disease patient being affected is four times greater than the general population.
  Although Alzheimer’s Disease most frequently occurs in elderly persons, it also afflicts a small number of younger patients (which suggests a genetic basis to some cases). Most cases of Alzheimer’s Disease are late in onset and are sporadic. A small percentage of cases of early in onset.
  
  CAUSES OF ALZHEIMER'S DISEASE
  These Substances Cause or Exacerbate Alzheimer's Disease
  
  Amino Acids
• Excessive levels of Aspartic Acid within the Brain may accelerate the development of Alzheimer's Disease.
• Excessive levels of Glutamic Acid within the Brain may accelerate the development of Alzheimer's Disease.
• Elevated Homocysteine contributes to the onset and progression of Alzheimer’s Disease.
  
  Antigens
• Elevated levels of Senescent Cell Antigen (SCA) are present on the neurofibrillary tangles and senile plaques that occur in the Brains of Alzheimer’s Disease patients.
  
  Enzymes
• Excessive production of Acetylcholinesterase (AChe) can exacerbate the symptoms of Alzheimer's Disease (by causing excessive destruction of Acetylcholine).
• Beta-Secretase (especially the Beta-Secretase 1 form) (a Proteolytic enzyme) catalyzes the conversion of Amyloid-Beta-Protein Precursor (APP) to Amyloid-Beta Protein (ABP) - the form of Amyloid that is strongly implicated in the onset and progression of Alzheimer’s Disease.
• Cyclooxygenase (COX-2 form) is involved in the progression of Alzheimer’s Disease (it may stimulate the release of Beta-Amyloid from Platelets).
• Excessive activity of Lipoxygenase (5-Lipoxygenase form) may be involved in the onset and progression of Alzheimer’s Disease (due to its role in the production of inflammatory Series 4 Leukotrienes).
• Excessive Monoamine Oxidase Type B (MAO-B) activity is implicated in Alzheimer's Disease.
  
  Food Additives
• Alzheimer's Disease patients should not consume Aspartame, as Aspartame can further exacerbate Alzheimer's Disease.
  
  Hormones
• Excessive Cortisol levels increase the rate of Neuron destruction in Alzheimer's Disease.
  
  Immune System Chemicals (Cytokines)
• Interleukin 1 (IL-1) may be implicated in the development and progression of Alzheimer’s Disease (it is involved in the promotion of genes for Amyloid-Beta-Protein Precursor (APP) (which is implicated in Alzheimer’s Disease)).
  Excessive production of Interleukin 6 (IL-6) is involved in the progression of Alzheimer’s Disease.
  
  Lipids
• The ApoE4 allele (form) of Apoprotein (e) is implicated in Alzheimer's Disease.
  
  - The ApoE4 allele is less prevalent in humans than the other ApoE alleles.
  - Late-onset Alzheimer's Disease patients are statistically (eight times) more likely to have the ApoE4 allele. It is speculated that ApoE4's association with Alzheimer's Disease arises not from any intricate toxicity but from the fact that people who inherit ApoE4 do not receive the protection against Alzheimer's Disease that ApoE3 provides.
  - 3% of humans carry two ApoE4 genes.
• Excessive Arachidonic Acid is speculated to be implicated in the development of Alzheimer’s Disease (due to its role as a precursor for the production of inflammatory Eicosanoids that may be implicated in Alzheimer’s Disease).
  
  Lipopigments
• Excessive accumulation of Lipofuscin occurs during the progression of Alzheimer’s Disease.
  
  Microorganisms
• Chlamydia pneumoniae may increase the risk of (late-onset) Alzheimer’s Disease (studies have demonstrated that Chlamydia pneumoniae is present in the regions of the Brain affected by Alzheimer’s Disease in 90% of late-onset Alzheimer’s Disease patients).
  
  Minerals
  Accumulation of Aluminium has been widely linked to Alzheimer's Disease:
  
  - Aluminium facilitates the toxic accumulation (aggregation) of Amyloid-Beta Protein (a known contributory factor to Alzheimer’s Disease).
  - Whenever the Brains of dead Alzheimer's Disease patients are dissected, researchers find Aluminium accumulated in them.
  - When injected into the brains of animals, Aluminium causes tangles of the Dendrites within the Brain.
  - Areas which use Aluminium Sulfate to purify drinking water, show increased incidence of Alzheimer's Disease.
  Mercury accumulation in the Brain from amalgam fillings is one of the primary causes of Alzheimer’s Disease.
  
  Proteins
• The Amyloid-Beta Protein form of Amyloid is believed to be the primary cause of the Cell death that occurs within the Brain during the progression of Alzheimer's Disease - it also contributes to the abnormal plaques, oxidative damage and Free Radicals within the Brains of Alzheimer's Disease patients:
  
  - When Amyloid-Beta is injected into the brains of rats, it destroys the same areas of the Brain as occurs during Alzheimer's Disease.
  - Defective Choline transportation combined with an increased propensity to autocannabalize Phosphatidylcholine from the Cell Membranes of Neurons activates the conversion of Amyloid-Beta-
  Protein Precursor (APP) to Amyloid-Beta Protein (ABP) within the Brains of Alzheimer's Disease patients:
  - This abnormal conversion of APP to ABP is theorized to occur when Choline transportation and Phosphatidylcholine autocannabalism is disturbed to the extent that APP is exposed to Proteolytic Enzymes (which APP is normally protected from) which catalyzes the conversion of APP to ABP
  
  Mutations in the Amyloid-Beta Protein Precursor (APP) Gene account for 5% to 20% of early-onset Alzheimer’s Disease.
  The Brains of Alzheimer’s Disease patients contain higher than normal levels of C-Reactive Protein (a biomarker of Inflammation).
  The presence of the gene for the ApoE4 allele of Apoprotein (e) correlates statistically with an increased risk of Alzheimer's Disease - this allele is believed to bind readily with Amyloid and subsequently transport Amyloid into the Brain where it may accumulate and precipitate the plaques that are implicated in Alzheimer's Disease.
  
  Alzheimer’s Disease patients exhibit far higher levels of SCA Auto-Antibodies (i.e. Auto-Antibodies to Senescent Cell Antigen) than normal, healthy persons.
  
  Toiletries
• The use of Aluminium-containing Antiperspirants has been associated with an increased risk of Alzheimer’s Disease.
  
  These Ailments Exacerbate Alzheimer's Disease
  
  Cardiovascular System
• Cerebral Insufficiency (impaired Blood Circulation to the Brain) is associated with Alzheimer’s Disease.
  
  Cells
• Damage to the Mitochondria of Brain Cells (especially damage to the Mitochondrial DNA of the Mitochondria) is one of the underlying causes of Alzheimer’s Disease.
  
  Immune System
• There is some evidence that Inflammation is an underlying factor in the onset and progression of Alzheimer’s Disease.
  
  Metabolism
• Excessive generation of Free Radicals in the Brain is one of the underyling causes of Alzheimer’s Disease.
  
  Musculoskeletal System
• Alzheimer’s Disease patients are at greater risk of (hip) Fractures than are normal, healthy people (this correlation between Alzheimer’s and hip Fractures is believed to be due to Vitamin D deficiency).
  
  Nervous System
• Alzheimer's Disease patients should not be subjected to excessive Stress (due to Stress causing the release of Cortisol that is implicated in Alzheimer's Disease).
  
  Alzheimer’s Disease Exacerbates these Ailments
  
  Nervous System
• The onset of Anosmia (impairment of the Sense of Smell) may be an early warning sign of Alzheimer's Disease.
• Periods of inappropriate Aggressiveness are a characteristic of the latter stages of Alzheimer’s Disease.
• Paranoia is characteristic of the latter stages of Alzheimer’s Disease.