There are now four drug treatments, all monoclonal antibodies, which have been shown to reduce amyloid in the brain. Amyloid build-up in the brain is associated with the cognitive changes of Alzheimer’s Disease, although there are questions about the exact nature of this relationship between amyloid and cognitive deterioration.
One of these drugs (lecanemab) has now been shown to halt or slow clinical deterioration in cognitive functions as well as reducing amyloid in the brain.
There are however, a number of ‘buts’:
1) The treatment and essential associated monitoring is complex and expensive. The treatments are given by intravenous infusion every second week for lecanemab, every four weeks for the other drugs. One early estimate of the cost of treatment, including essential MRI monitoring and other tests was AUD 72,000 per year!
2) The clinical effects of lowering brain amyloid are not huge. This is probably because, as confirmed by post-mortem studies of Alzheimer’s disease, ‘plaque and tangle pathology likely accounts for less than 50% of cognitive impairment, with most remaining variance explained by other pathologies (eg. cerebrovascular disease, TDP-43, and alpha-synuclein)’*.
3) Some people (about 20%) given these treatments experience ‘Amyloid-related imaging-abnormalities’ ARIAs. These are microscopic haemorrhages or oedema which can be detected on MRI without symptoms but in a very small number of people they can result in symptoms. Temporary or permanent cessation of the treatment generally allows these haemorrhages or oedema to disappear.
4) These treatments are only likely to be helpful for people with early or minor cognitive impairment due to Alzheimer’s disease. There has been a general realization that there is usually a long lead-in time, of many years, to development of clinical dementia in Alzheimer’s disease.
*A Step Forward in the Fight Against Dementia—Are We There Yet? | Dementia and Cognitive Impairment | JAMA Neurology | JAMA Network