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Therapeutics

Much behind disease pathology remains unclear, and research and developments are approaching therapeutic treatments from various directions. As a result, the routes to commercially available treatments are highly diverse. There are currently over 200 compounds in development for AD, with 50 in late-stage trials. The current late-stage product pipeline, however, features few original drugs, with most being marginal improvements on currently available drugs.

Drugs in development generally consist of improved Acetylcholinesterase inhibitors (AChEI s) and amyloid-β modulators, though there are numerous others with unique mechanisms of action. NeuroDelta believes that AChEI's are unlikely to revolutionize the field, and generally only treat symptoms, not the underlying disease. However, these drugs could still be useful if they offer longer-term effects or have less severe side effects. Beta-Modulatorstry to disrupt the behaviour thought to be the underlying cause of AD under the Amyloid Hypothesis: a chronic imbalance between amyloid-β production and amyloid-β clearance. However, the point at which amyloid production and deposition is affected could be absolutely key to discovering a successful therapy. Because of the lack of evidence showing amyloid-β is overproduced in AD, its production is likely to be normal (and necessary), and any compound that prevents its formation could have major side effects.

In actuality, most drugs in development fail to address the underlying pathology of AD and look only to modulate the diseases symptoms. Furthermore, few have progressed to advanced stages and there does not appear to be a single wonder drug in clinical development that addresses the markets real needs.

NeuroDelta has developed a number of compounds that it hopes will prove effective at preventing further development of AD. The compounds target key elements in the progress of the disease and work in a different manner to any other potential treatment becuase of our unique understanding of the role of phosphorylated amyloid-β.