World Alzheimer’s Day: Promising Advances in Alzheimer’s Disease Research

21st September 2024

By Samantha Weetman, Science Writer.

Every year, World Alzheimer’s Day on September 21st serves as a reminder of the ongoing battle against Alzheimer’s disease (AD) and the need for increased awareness, research, and support for patients and caregivers. Dementia affects over 55 million people globally, and Alzheimer’s is the most common form. As the aging population continues to grow, the number of people impacted by AD is expected to rise significantly. However, amidst the challenges posed by this neurodegenerative disease, recent developments in research are providing new hope for potential treatments and a better understanding of the disease.

While there are over 100 ongoing AD clinical trials [1], this blog highlights just a few recent promising advances in Alzheimer’s research, offering renewed optimism in the fight against this devastating condition.

Breakthrough in Monoclonal Antibody Therapies

Monoclonal antibodies have long been investigated for their potential to target the amyloid plaques that build up in the brains of Alzheimer’s patients. In 2024, two anti-amyloid monoclonal antibodies, donanemab and lecanemab, have been in the spotlight for their ability to slow cognitive decline in early-stage AD patients.

Lecanemab, recently approved in the UK, has been shown to significantly reduce amyloid plaques and slow the progression of cognitive symptoms. Lecanemab currently remains unavailable on the NHS, but despite ongoing debates about its long-term safety and efficacy, it marks a key step in Alzheimer’s treatment [2]. In the US, donanemab has demonstrated similar promising results, particularly in reducing clinical decline in AD patients [3].

Interestingly, studies have found that these anti-amyloid-β (Aβ) monoclonal antibodies not only reduce amyloid plaques but also increase levels of a key protein, 42-amino acid isoform amyloid-β (Aβ42), which is associated with better cognitive outcomes. A meta-analysis of 24 clinical trials involving over 25,000 Alzheimer’s patients found that increases in cerebrospinal fluid Aβ42 were linked to slower cognitive decline, offering more support for anti-amyloid treatments [4].

Chaperone Therapy: A New Approach to Restoring Cognitive Function

An exciting development in Alzheimer’s treatment is chaperone therapy, which restores protein balance in the brain. In a study published in late 2023, researchers demonstrated that supplementing protein chaperones in an amyloid precursor protein knock-in AD mouse model improved cognitive function and reduced amyloid-β levels.

Chaperone therapy boosts the body’s ability to manage misfolded proteins, which are a hallmark of Alzheimer’s pathology. The study found that chaperone supplementation increased the activity of XBP1s and ADAM10, key proteins involved in maintaining protein homeostasis and reducing amyloid-β production. Remarkably, even late-stage interventions showed positive results, improving learning and memory in the treated mice [5].

These findings suggest that chaperone therapy could be a valuable tool in restoring brain function and slowing Alzheimer’s disease progression, potentially offering a new avenue for therapeutic development in humans.

Calcium Channel Blockers to Improve Blood Flow in the Brain

New research published in September 2024 has revealed the potential of calcium channel blockers in improving cerebral blood flow in Alzheimer’s patients [6]. Alzheimer’s disease is often accompanied by reduced blood flow to the brain, leading to increased hypoxia and worsening cognitive function. Researchers found that blocking L-type voltage-gated calcium channels can help relax pericytes (contractile cells in capillaries), improving microvascular blood flow and reducing immune cell stalling.

In the study conducted on Alzheimer’s disease model mice, treatment with the calcium channel blocker nimodipine improved blood flow and oxygen levels in the brain, which helped alleviate the cognitive symptoms of AD [6]. This approach could offer a new therapeutic strategy to enhance brain energy supply and potentially improve cognition in Alzheimer’s patients.

Stem Cell and Gene Therapy Research

Stem cell research is unlocking new possibilities for treating Alzheimer’s disease. One promising avenue involves hematopoietic stem cell (HSPC) gene therapy. A study published in September 2024 demonstrated that transplanting of genetically modified HSPCs into the central nervous system (CNS) significantly reduced Aβ aggregation and neuroinflammation in AD mouse models [7].

These modified cells differentiated into microglia-like cells, which help to clear amyloid plaques. The therapy also improved memory and cognitive function in the mice. While the approach is still in its early stages, the results highlight the potential of gene therapy as a future therapeutic strategy for treating Alzheimer’s disease, especially in addressing neuroinflammation.

Harnessing Antioxidants to Target Amyloid Plaques

Another recent study explored using antioxidants to counter the oxidative stress that contributes to Alzheimer’s disease progression. Researchers developed a metal-organic framework (MOF) combined with curcumin, a potent antioxidant, to create a system capable of scavenging Aβ plaques and reducing oxidative stress in Alzheimer’s model mice [8].

This novel treatment slowed cognitive decline by breaking down existing amyloid plaques and preventing the formation of new ones. The antioxidant system also demonstrated strong neuroprotective effects without causing toxicity, making it a promising candidate for future Alzheimer’s therapies [8].

Looking Ahead: Hope on the Horizon for Alzheimer’s Treatment

The recent advances in Alzheimer’s research are providing new hope for slowing or reversing this debilitating disease. Monoclonal antibody treatments, chaperone therapy, calcium channel blockers, stem cell therapies, and innovative antioxidant systems all show promise in addressing the root causes of Alzheimer’s.

While more research is needed to confirm these findings and bring treatments to market, these developments mark significant steps forward in the fight against Alzheimer’s disease. As we mark World Alzheimer’s Day, it’s important to reflect on the progress made and continue supporting research that could lead to life-changing breakthroughs for millions of people.

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References

1]         J. Cummings, Y. Zhou, G. Lee, K. Zhong, J. Fonseca, and F. Cheng, “Alzheimer’s disease drug development pipeline: 2024,” Alzheimer’s & Dementia: Translational Research & Clinical Interventions, vol. 10, no. 2, p. e12465, Apr. 2024, doi: 10.1002/TRC2.12465.

[2]        “Beyond lecanemab: unravelling the future of Alzheimer’s treatments – Alzheimer’s Research UK.” Accessed: Sep. 18, 2024. [Online]. Available: https://www.alzheimersresearchuk.org/news/beyond-lecanemab-unravelling-the-future-of-alzheimers-treatments/

[3]        “New Alzheimer’s drug, donanemab – what is it and how does it work? – Alzheimer’s Research UK.” Accessed: Sep. 18, 2024. [Online]. Available: https://www.alzheimersresearchuk.org/news/new-alzheimers-drug-donanemab-what-is-it-and-how-does-it-work/

[4]        J. Abanto, A. K. Dwivedi, B. P. Imbimbo, and A. J. Espay, “Increases in amyloid-β42 slow cognitive and clinical decline in Alzheimer’s disease trials,” Brain, vol. 139, no. 4, pp. 16–17, 2012, doi: 10.1093/BRAIN/AWAE216.

[5]        J. M. Hafycz, E. Strus, K. Sengupta, and N. Naidoo, “Early and Late Chaperone Intervention Therapy Boosts XBP1s and ADAM10, Restores Proteostasis, and Rescues Learning in Alzheimer’s Disease Mice,” Aging Biology, vol. 1, no. 1, p. 20230017, Dec. 2023, doi: 10.59368/AGINGBIO.20230017.

[6]        N. Korte et al., “Inhibiting Ca2+ channels in Alzheimer’s disease model mice relaxes pericytes, improves cerebral blood flow and reduces immune cell stalling and hypoxia,” Nature Neuroscience 2024, pp. 1–15, Sep. 2024, doi: 10.1038/s41593-024-01753-w.

[7]        R. Milazzo et al., “Therapeutic efficacy of intracerebral hematopoietic stem cell gene therapy in an Alzheimer’s disease mouse model,” Nature Communications 2024 15:1, vol. 15, no. 1, pp. 1–20, Sep. 2024, doi: 10.1038/s41467-024-52301-w.

[8]        K. Liu et al., “Interface potential-induced natural antioxidant mimic system for the treatment of Alzheimer’s disease,” Communications Chemistry 2024 7:1, vol. 7, no. 1, pp. 1–6, Sep. 2024, doi: 10.1038/s42004-024-01299-9.