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The War on Alzheimer’s

Updated: Mar 9, 2023

For 30 years Alzheimer’s researchers have been investigating a specific method of therapy proposed by leading researchers of the disease and have seen a 100% failure rate, until now. A monumental study pertaining to the use of ‘lacanemab’ to treat the most common form of dementia was announced at the Clinical Trials on Alzheimer’s Disease conference (CTAD) in San Francisco and simultaneously published in The New England Journal of Medicine, with both detailing the successful effects of the drug. Prior to this study there were no drugs known to alter the course of the disease [2]. Research groups around the world have praised the release of these findings which have been making global headlines in recent days, with Alzheimer’s Research UK heralding the results as “momentous” [2]. Let’s break down what exactly these findings have shown..

In a brain with Alzheimer’s disease, the protein fragment beta-amyloid deposits in the gaps between neurons leading to the formation of plaques on the nerve cells. Studies show that people commonly develop plaques with age but those with Alzheimer’s have shown to develop plaques in a certain pattern, most prominently beginning in areas of the brain important for memory prior to spreading throughout the organ. However, there is a persistent gap in clinical knowledge of the disease and it remains unclear exactly how the causation of Alzheimer’s is linked to these plaques. It is widely theorised that the plaques critically block communication between nerve cells, disrupting necessary cell survival processes and ultimately leading to the destruction of the cells, eliciting symptoms such as personality changes, memory failure, and problems with the undertaking of normal daily tasks [3]. 30 years ago, leading researchers proposed the targeting of beta-amyloid proteins in the brain, and at the 15th Annual Clinical trials on Alzheimer’s Disease on November 29th to December 2nd, 2022, scientists revealed they had finally reached a breakthrough clinical finding [5].

Lecanemab has been proven to have “reduced markers of amyloid in early Alzheimer’s disease and resulted in moderately less decline on measures of cognition and function than placebo” [1] according to the New England Journal of Medicine following an 18-month long clinical trial on nearly 1,800 participants. These participants, all between the ages of 50 to 90 years old, were randomly arranged into two groups of which one group underwent the administration of intravenous lecanemab and the other a placebo, both of which occurred fortnightly. Participants were then closely monitored and clinically rated on a symptom based 18-point scale ranging from normal through to severe levels of dementia, with those receiving lecanemab rating a statistically significant 0.45 points better than those who received the placebo. Results also showed that those who were administered the drug experienced a reduction in the rate of cognitive decline by 27% [4]. Lecanemab works in the brain as an antibody, sticking to the cognitively destructive amyloid proteins and attracting immune cells towards the neurons to break down the harmful proteins, resulting in a recused amount of proteins clustering the nerve cells. A doctor working at North Bristol NHS Trust, Dr Elizabeth Coulthard, says that "people have, on average, six years of living independently once mild cognitive impairment starts. Slow that decline by a quarter and it could equate to an extra 19 months of independent life, ‘but we don't know that yet’” [2]. Lecanemab is not by any means a cure, but rather aids in slowing the progression of Alzheimer’s in its very early stages. This earliness in identifying memory problems crucial to lecanemab’s use is very rarely detected, with only 1-2% of people with dementia being referred for amyloid tests - brain scans or spinal fluid analyses - that are necessary to recognise Alzheimer’s early enough [2]. It is important to emphasise that whilst this historical breakthrough is indeed momentous, it is only a minuscule victory in the war against Alzheimer’s disease. 

The New England Journal of Medicine was careful to highlight in their conclusion also the adverse side-effects this drug is likely to induce as well as noting the need for longer trials to determine the efficacy and safety of the drug for use against early Alzheimer’s disease. Throughout the trials participants underwent routine brain scanning, with 17% experiencing brain bleeds and 13% experiencing brain swelling. 7% of participants had to discontinue use of lecanemab as a result of side-effects they experienced [2]. Most side effects are “mild to moderate” [4], said Dr. Marwan Sabbagh of the Barrow Neurological Institute, who gave a presentation on lecanemab's safety. Overall it is evident that patients must be assessed on an individual basis to resolve whether the benefits outweigh the posed risks of the drug. However, scientists say we are a long way from any form of distribution of the drug with much more in depth and long-term testing required as well as wide-spread expansion in testing for the disease. 

By 2025, 1 million people will be living with the condition in the UK with many millions more carers, partners, families and friends affected by the care necessary to deal with the debilitating and immobilising symptoms of the disease [6]. Over half of the UK population know someone who has been diagnosed with some form of dementia and just under half of the UK view dementia as the most frightening condition they could develop in the future, a figure which has risen by 7% between 2018 and 2021 [7]. The imagined and real impact of dementia diseases, including Alzheimer’s, is a blatant indication of the need for continued research to fill the gaps in expert knowledge. This clinical publication pertaining to lecanemab is utterly significant, despite the considerable risks posed and a need for further research. There is a persistent and severe lack of adequate testing, treatment and equality of care across the country and the globe. Therefore any advances made in this field of research, in which breakthroughs appear few and far between, are of paramount importance, and so though this may be but a minuscule victory in the war against Alzheimer’s disease it is indeed a victory nonetheless. 

The views stated in the above article are that of the author ELIZABETH KEEN, not TEDxWarwick nor TED.

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