There is no still no scientific consensus on the causal mechanism of Alzheimer’s disease, or at least on the correct target for medicinal intervention – the four main contenders are:
(a) build-up of amyloid-beta fibrils
(b) build-up of tau protein tangles
(c) inflammation in the brain
(d) reaction to a virus infection
The Bad News: Last week the antibody drug “aducanumab” was withdrawn from clinical trials because of poor results – this was an anti-amyloid-beta drug. This follows other disappointing drugs aimed at amyloid-beta.
The Good News: However today there has been more positive news – a drug which has already been approved for clinical use against Hepatitis-D, called Lonafarnib, has been found to dramatically ameliorate the progress of dementia in a mouse model of the disease. The drug seems to block an enzyme (called farnesyltransferase) that facilitates the activity of the protein Rhes ultimately enhancing lysosome activity. Lysosomes are cellular waste-clearance systems that break down the toxic proteins, including tau. Research into this pathway and mechanism may open the door on further possible drugs.