β-Amyloid in Alzheimer’s Disease: Therapeutic Implications

Recent evidence has been accumulating to suggest that the peptide β-amyloid may be implicated as a causative agent in Alzheimer’s disease. This compound is known to accumulate in the cerebral plaques that are characteristic of the disease. Whether β-amyloid is toxic per se is yet to be established, but several options are available which may reduce the toxicity of the agent and, thus, have potential in the treatment of Alzheimer’s disease. Prevention of the generation of β-amyloid from the amyloid precursor protein (APP) and inhibition of the possible neurotoxic effects of the compound are being explored. A recent finding that has gained much attention is that β-amyloid can form ion channels that are cation-specific. An increase in intracellular calcium levels can occur via these channels, which may be neurotoxic and cause inflammatory responses. The use of channel blocking agents, such as trometamol (tromethamine), may prevent neurotoxicity, while anti-inflammatory drugs may also prove to be useful therapeutic agents.