Alzheimer’s disease is a neurodegenerative disease commonly known for causing memory loss. It also can cause behavioral changes and cognitive deterioration[1]. Nearly 1 million people today are living with Alzheimer’s disease in the UK. As the aging population increases, some estimate 1.2 million people, living with Alzheimer’s by 2024 in England and Wales, whilst recent estimates from UCL suggest much higher numbers - 1.7 million people[2]. With an increase in the number of cases, with current costs estimated between £23 billion a year costs are predicted to triple from £45.4billion by 2040 (in terms of care costs)[3]. 

Recent trials have shown that donanemab (an antibody drug) helps to rapidly remove the beta-amyloid protein, which is said to have a significant role in progressing Alzheimer’s. According to the Lancet, the drug, after undergoing global clinical trials, has been found to slow the rate of cognitive decline by a third[4]. Many are sure that the discovery of this drug is a step forward in finding an effective cure for Alzheimer’s disease in the future[5].

However, though beta-amyloid may be an obvious target for drug treatment, causes of Alzheimer’s disease further research (only risk factors are known). For example, the role of glial cells still requires some further investigation. Research into the disease has been focused mainly on neurons and their degeneration. However, glial cells are said to have significant functions in the central nervous system, maintaining homeostasis and the structure of neurons[6]. So far, the physiological decline in the glial cells, particularly microglial cells) and the decline in the age development of the brain is similar to the decline in the developmental function of the brain in Alzheimer’s disease[7]. The deterioration stimulates the release of inflammatory cytokines, which have adverse effects on the neurons[8]. Perhaps targeting this mechanism could provide a new target for the treatment of Alzheimer’s disease.

Additionally, though, the effectiveness of many Alzheimer’s treatments (specifically new antibody treatments targeting beta-amyloid) relies on the early diagnosis of Alzheimer’s in patients. That poses an added cost for specialist scans to be made readily available, as well as the drug costs for the NHS, only 2% of people with dementia receive either of these gold-standard methods of diagnosis. An estimated 28,000 people a year could miss out on treatments without proper access to diagnosis for early onset Alzheimer's[9]. 

To conclude, though recent Alzheimer’s treatments may be significant in discovering a cure for the disease, there are still profound gaps in our understanding of the fundamental causes of it. The drugs also need more investigation into their side effects:

Brain swelling (ARIA-E) was seen on the scans of one in four participants, with one in 20 experiencing symptoms, and less than two in every 100 participants experienced serious brain swelling after taking donanemab[10]. Additionally, the new drugs rely on better accessibility to diagnosis assessments for the disease which would inflate the cost for the NHS, but may perhaps reduce the cost of care in the future (should cost be budgeted effectively).

References

1. Alzheimer’s disease (2024) Yale Medicine. Available at:

https://www.yalemedicine.org/conditions/alzheimers-disease (Accessed: 23 April 2024).

2. Chen, Y. ed., (2023). Dementia incidence trend in England and Wales, 2002–19, and projection for dementia burden to 2040: analysis of data from the English Longitudinal Study of Ageing. [online] The Lancet Public Health. Available at: https://www.thelancet.com/journals/lanpub/article/PIIS2468-2667(23)00214-1/fulltext [Accessed 13 May 2024].

3. Society, A. (ed.) (2023) What are the costs of dementia care in the UK?,

Alzheimer’s Society. Available at: https://www.alzheimers.org.uk/about-us/policy-

and-influencing/dementia-scale-impact-numbers (Accessed: 23 April 2024).

4. Alawode, D.O.T., Heslegrave, A.J., Fox, N.C. and Zetterberg, H. (2021). Donanemab removes Alzheimer’s plaques: what is special about its target? The Lancet Healthy Longevity, [online] 2(7), pp.e395–e396. doi:https://doi.org/10.1016/s2666-7568(21)00144-6.

5. Ibid

6. Nirzhor, S., Khan, R. and Neelotpol, S. (2018). The Biology of Glial Cells and Their Complex Roles in Alzheimer’s Disease: New Opportunities in Therapy. Biomolecules, [online] 8(3), p.93. doi:https://doi.org/10.3390/biom8030093.

7. Hanisch, U.-K. and Kettenmann, H. (2007). Microglia: active sensor and versatile effector cells in the normal and pathologic brain. Nature Neuroscience, [online] 10(11), pp.1387–1394. doi:https://doi.org/10.1038/nn1997.

8. Streit, W.J. and Xue, Q.-S. (2009). Life and Death of Microglia. Journal of Neuroimmune Pharmacology, [online] 4(4), pp.371–379. doi:https://doi.org/10.1007/s11481-009-9163-5.

9. BBC: Panorama (2024). BBC Panorama captures the promise and challenges of new Alzheimer’s treatments. [online] Alzheimer’s Research UK. Available at: https://www.alzheimersresearchuk.org/news/bbc-panorama-captures-the-promise-and-challenges-of-new-alzheimers-treatments/ [Accessed 13 May 2024].

10. Ibid

Written by Paris L.

Moderated by Joanna