Alzheimer's Disease - Causes

These Substances may Cause or Exacerbate Alzheimer's Disease

Amino Acids

 Excessive levels of Aspartic Acidwithin the Brain may accelerate the development of Alzheimer's Disease.  ^[1]

 Excessive levels of Glutamic Acidwithin the Brain may accelerate the development of Alzheimer's Disease.  ^[2]

 Elevated Homocysteine contributes to the onset and progression of Alzheimer's Disease.  ^[3]

Antigens

 Elevated levels of Senescent Cell Antigen (SCA) are present on the and senile plaques that occur in the Brains of Alzheimer's Disease patients.

Carbohydrates

 Excessive consumption of dietary Carbohydrates may increase the risk of Alzheimer's Disease:  ^[4]

 Excessive consumption of Sucrose may increase the risk of Alzheimer's Disease.  ^[5]

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.  ^[6]

 Cyclooxygenase (COX-2 form) is involved in the progression of Alzheimer's Disease (it may stimulate the release of Beta-Amyloid from Platelets).  ^[7]

 Excessive activity of Glycogen Synthase Kinase-3 may be implicated in Alzheimer's Disease (it is involved in the production of the that are a feature of Alzheimer's Disease).  ^[8]

 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).  ^[9]

 Excessive Monoamine Oxidase Type B (MAO-B) activity is implicated in Alzheimer's Disease.  ^[10]

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.  ^[11]

 Excessive Insulin production or release (hyperinsulinemia) may increase the risk of Alzheimer's Disease:  ^[12]

 Although optimal Brain Insulin levels may reduce the risk of 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)).  ^[13]

 Excessive production of Interleukin 6 (IL-6) may be involved in the progression of Alzheimer's Disease.  ^[14]

 Elevated levels of Tumor Necrosis Factor (TNF) and increased release of TNF in the Brain may occur in Alzheimer's Disease patients.This increased TNF activity may contribute to the death of Neurons in the Brain of Alzheimer's Disease patients.  ^[15]

Lipids

 The ApoE4 allele (form) of Apoprotein (e) is implicated in Alzheimer's Disease:  ^[16]

 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.