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The Bad News: Last week the antibody drug “aducanumab” was withdrawn from clinical trials because of poor results – this was an anti-amyloid-beta drug.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.
Update 29th May 2019: Research published today seems to have established the mechanism by which the Herpes virus can facilitate Alzheimers. Essentially proteins from fluids within the body tend to stick to the virus surface, comprising what is termed a protein corona. It seems that there is enzymatic activity within that corona that facilitates the aggregation of amyloid plaques. It is suggested that this may not be the only causal factor leading to Alzheimers but certainly is capable of speeding up the disease process.