Amyloid-Beta Protein

Overview

Amyloid-Beta Protein essential for normal day-to-day information transfer through nerve cell networks in the brain is found in excess in the brains of Alzheimer''s disease sufferers.

Toxic Effects of Amyloid-Beta Protein

Cells

 Amyloid-Beta Protein may cause oxidative damage to the Deoxyribonucleic Acid (DNA) content of the Mitochondria (i.e. mitochondrial DNA) of Cells.  ^[1] 

Nervous System

 Amyloid-Beta (after its activation by APP) is believed to be the primary cause of the Cell death, Amyloid plaques, oxidative damage and Free Radical generation that occurs within the Brain during the progression of Age-Associated Memory Impairment, Alzheimer''s Disease ^[2] and Down''s Syndrome:

 When Beta-Amyloid is injected into the Brains of rats, it destroys the same areas of the Brain that are damaged during the progression of Alzheimer''s Disease.

 Amyloid-Beta Protein may destroy Neurons:  ^[3]

 Amyloid Beta-Protein may destroy Cholinergic Receptors on Cholinergic Fibers.  ^[4]

 Excessive Amyloid-Beta Protein in the Hippocampus of the Brain may interfere with Short-Term Memory.  ^[5]

Amyloid-Beta Protein may Interfere with these Substances

Nucleic Compounds

 Amyloid-Beta Protein may cause oxidative damage to the Deoxyribonucleic Acid (DNA) content of the Mitochondria (i.e. mitochondrial DNA) of Cells.  ^[6]

These Substances may Reduce the Toxic Effects of Amyloid-Beta Protein

Alkaloids

 Huperzine A may counteract the neurotoxic effects of Amyloid-Beta Protein.  ^[7]

Amino Acids

 Acetyl-L-Carnitine (ALC) may reduce the toxicity of Amyloid-Beta Protein to Neurons.  ^[8]

 Agmatine may inhibit the ability of Amyloid-Beta Protein to cause Memory impairment.  ^[9]

 Taurine may reduce the toxicity of Amyloid-Beta Protein.  ^[10]

Carbohydrates

 Fucoidan may reduce the toxicity of Amyloid-Beta Protein.  ^[11]

Carotenoids

 Beta-Carotene may counteract the toxicity of Amyloid-Beta Protein.  ^[12]

Enzymes

 Alpha-Secretase catalyzes the conversion of Amyloid-Beta Protein into two inert compunds.  ^[13]

Growth Factors

 Insulin-like Growth Factor-1 (IGF-1) may facilitate the removal of Amyloid-Beta Protein from the Brain.  

 Transforming Growth Factor-beta (TGF-beta) may stimulate Microglia to clear Amyloid-Beta Protein from the Brain.  ^[14]

Hormones

 DHEA (Dehydroepiandrosterone) may reduce the accumulation of Amyloid-Beta Protein and may reduce the toxic effects of Amyloid-Beta Protein.  ^[15]

Estradiol (both the Estradiol 17-Alpha and the Estradiol 17-Beta forms of Estradiol) may inhibit the ability of Amyloid-Beta Protein to destroy Neurons.  ^[16]

 Melatonin may block the oxidative damage caused to the Deoxyribonucleic Acid (DNA) content of the Mitochondria (mitochondrial DNA) caused by Amyloid-Beta Protein.  ^[17]

 Pregnenolone may reduce the toxic effects of Amyloid-Beta Protein.  ^[18]

 Testosterone may help to reduce the endogenous production of Amyloid-Beta Protein.  ^[19]

Lignans

 Sesaminol may inhibit the ability of Amyloid-Beta Protein to kill Neurons.  ^[20] 

Lipids

 Docosahexaenoic Acid (DHA) may facilitate the removal of Amyloid-Beta Protein by increasing Transthyretin levels.  ^[21]

 Eicosapentaenoic Acid (EPA) may counteract the toxicity of Amyloid-Beta Protein.  ^[22] 

Minerals

 Copper may inhibit the production of Amyloid-Beta Protein:  ^[23]

 Normally, Copper is bound to Amyloid-Beta-Precursor Protein (APP), preventing its conversion to Amyloid-Beta-Protein.  Depleted Copper levels in the Brain may reduce Copper binding to APP.  When Copper is not present in APP, APP becomes free to convert to Amyloid-Beta Protein.  Copper supplementation may thereby help to prevent the conversion of APP to Amyloid-Beta Protein.