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The Hopeful Future Of Alzheimers Disease: Research & Treatments
Although pathophysiology is a science, it also designates suffering in people; the clinician should never lose sight of this aspect of its definition. (McCane and Huether, 2019). Pathophysiology is a realm of science which encompassess the harmful effects of disease on the human body. As a future RN, I find great importance in this study and recognize the potential current research and understanding of disease has to increase the length and quality of life. As a nurse, I will be responsible for providing support, encouragement and comfort to not only my patients, but their families who are also affected by the impairments of disease. In this role, staying current about new technologies and treatments available to cure illness or treat symptoms will be essential in providing care. One illness which devestates the lives of many today is Alzheimers Disease (AD).
Along with over 26 million individuals diagnosed with Alzheimers disease worldwide, stands their families and loved ones (Cao et al. 2018). I am one of many individuals who has been personally affected by (AD). My Nana was diagnosed last year, although we had noticed signs much sooner. She still remains relatively independent, but her condition is worsening as she has now lost the ability to cook and drive. I know the progressive disease will continue to deteriorate her memory and physical ability, which is why I am passionate about the current efforts to slow or reverse these effects. Current attempts and studies being conducted by researchers to find a cure or new treatment options have provided me with hope for the furture of Alzheimers Disease.
Targeting Amyloid
One of the hallmark signs of AD is the insoluble accumulation of Beta-Amyloid referred to as amyloid plaques. The formation of these plaques occurs before symptoms appear and worsen as the disease progresses. One of the major attempts of slowing Alzheimers has been geared towards targeting amyloid-beta via inhibitors and immunizations. Amyloid-Beta originates from Amyloid precursor protein (APP) which is cleaved by enzymes. Researchers thought that if they can inhibit this process, it can decrease the devastating effects of amyloid. BACE1 inhibitors have shown to reverse amyloid deposition and improve cognitive function in a mouse model with 5x Familial AD (FAD) transgenic background (Cao et al. 2018). However, when tested on adults, this inhibitor did not work quite as effectively. Cao and others (2018) believe that conducting more studies to identify the optimal timing to use BACE1 inhibitors will increase efficacy. In my opinion, this attempt is not a failure because with more research, it could potentially be an effective method if utilized in the correct population.
In addition, passive immunizations against amyloid-beta may be the future of AD treatment. BAN2401 acts on soluble amyloid beta protofils. In a study conducted by Cao and others (2018), 18 months of treatment with a large dosage conveyed decreased clinical progression and amyloid accumulation. ApoE4+ carriers were excluded from this dosage, but the findings remain significant because BAN2401 still provided positive effects for others. There are currently more efforts to target ApoE, which will provide even more opportunities for carriers of ApoE4+ to still recieve effective treatment as medicine advances. Another passive vaccine, Aducanumad, aimed to decrease amyloid plaques (Cao et. al. 2018). It was successful for individuals with prodromal and mild Alzheimers. This also showed a delayed cognitive decline (Cao et. al. 2018). While none of these treatments provide a definitive cure, the failures of targeting amyloid has pushed researchers to dig deeper and seek how to attack other components of this multifactorial disease leading us closer to answers. It should also be noted that different treatments may work better for certain individuals depending on how far the AD has progressed. Overall, these efforts should not be discreditied regardless of the outcome.
Therapy Options Targeting Tau Proteins
Tau protein aggregates make up neurofibrillary tangles (NFTs), another clinical manifestation of AD. It is now thought that Tau accumulation may potentially have a larger effect on cognitive decline seen in AD than amyloid-beta (Cao et. al. 2018). There are many approaches being taken to interupt the creation of Taus NFTs, but O-GlcNAcase inhibitors appear to create immense hope as it prevents the enzyme from stripping sugar from the Tau protein. Animal studies have been successful with the use of this inhibitor showing a prevention of NFTs, increased neuron survival and decrease of tau phosphorylation (Cao et. al. 2018). These results are significant because decreasing neuron loss will coincide with a decrease of devastating symptoms that AD brings about. I am especially excited to see how research progresses with these findings as it enters human clinical testing.
Symptomatic Treatment: Serotonin 6 (5-HT6) receptor
Today there are symptomatic treatment options on the market such as Memantine and acetylcholinersterase inhibitors which act to reduce the loss of ACh and correct the imbalance of glutamergic signaling. (Jong & Mork, 2017). These medications have been successful at improving cognition, function and even selected behavioral symptoms in AD patients. (de Jong & Mork, 2017). While great strides have been made in symptomatic treatment for AD, researchers are still working diligently to identify more methods to improve the lives of not only Alzheimers patients, but their caregivers and family as well.
One route scientists are eager to further explore is the atagonism of the serotonin 6 receptor. In AD, research has supplied evidence that the serotonergic system breaks down which ultimately affects an individuals learning and memory. In addition, it has been shown that there is an imbalance of excitation and inhibition among neurons which contributes to the slowing cortical EEG seen in Alzheimers patients (de Jong & Mork, 2017). Idalopiridine, a serotonin 6 receptor antagonist, was able to enhance the neuronal network oscillations of the frontal cortex in rats and had a synergistic effect when combined with donepzil (de Jong & Mork, 2017).
A functional magnetic resonance imaging was performed on awake rats to indicate how many brain regions Idalopiridine and donepezil activiate alone and together. Alone Idalopiridine activated only 8 brain regions, donepezil activated 19, but when administered together they collectively activated 36 brain regions (de Jong & Mork, 2017). The combination also appears to reap many benefits by raising ACh levels significantly. This information is relevant for AD patients because it provides insight to how this additive effect may create a new combination therapy which can allieviate symptoms pertaining to cognition, emotion, motivation, learning and memory.
Conclusion
The options discussed above are just a few of the countless efforts researchers have devoted to bettering the future of Alzhiemers treatment. Each failure has presented a new found victory which improves the lives of many patients, caregivers and family members who endure the exhaustion and devastation that AD carries. As we look into the future of Alzheimer medications, I think it has been made very clear researchers will not quit until they have exact answers on how to best treat this multifactorial disease. In addition, there are currently FDA approved drugs which already provide some benefit to AD patients so adding to those already positive effects can only provide a brighter future.
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