top of page
Medicine4Youth
Jul 26, 20207 min read

Alzheimer's Diseases

Updated: Jul 30, 2020

CAUSES, SYMPTOMS, AND TREATMENTS


Sultana Yeasmin

 


Millions of people around the world feel the pain of watching their loved ones slowly lose their memories and other cognitive functions right before their eyes, due to neurological conditions. One example is Alzheimer’s Disease (AD), a common neurodegenerative disorder that deteriorates neurons and causes them to die off. The disease is extremely serious and usually fatal, but with the help of regular treatments, can be managed. The disorder is unfortunately prevalent in an astonishing number of people around the world, and definitely something truly worth grasping.

 

CAUSES

Scientists believe that there is no single reason for one to obtain Alzheimer’s disease. They believe it’s a mix of many different factors, such as genetics, age, and one’s lifestyle. Even so, just like any other illness, there is always a hunt for the science behind the disease. While the biology of this phenomenon is still unclear, researchers have realized that the problem is with “brain proteins that fail to function normally, disrupt the work of brain cells (neurons) and unleash a series of toxic events” (Alzheimer’s Disease). In addition, through recent studies, scientists have tracked down two main biomarkers that are correlated to AD.

The first concept that links to the disease is the deposition of amyloid plaques within the brain’s structures. These amyloid plaques are composed of beta amyloid peptides (Aβ), which are actually broken fragments of a protein called amyloid precursor proteins (APP). APP’s correlation to Alzheiner’s disease is still not completely understood by scientists yet, but they do know that the protein is generally beneficial and needed for neural development and synapse formation (Nicolas et al., 2014). The beta amyloid in the brain of an Alzheimer’s patient is misfolded, so that it isn’t properly processed by the brain (Rajasekhar et al., 2015). Through this, all the Aβ builds up together into plaques around neurons, creating a toxic reaction from the brain, which scientists are still trying to figure out why. These amyloid plaques then lead to apoptosis, or programmed cell death, which continuously progresses the disease in a patient’s brain (Loo et al., 1993).

The second concept that relates to Alzheimer’s is the prevalence of neurofibrillary tau tangles (NFTs) in the brain. The proteins usually play a major role in stabilizing the axons and microtubules of a neuron (Avila et al., 2016), but that’s not the case when it comes to Alzheimer’s. Hyperphosphorylated tau proteins lead to changes in how the proteins are regularly processed by the brain. As a result, clumps of tau proteins are formed, better known as NFTs. Since there is a prevalent amount of tau tangles, neurons fail to support their own structure (Iqbal et al., 2011). Along with all of this, the NFTs also “block the neuron’s transport system, which harms the synaptic communication between neurons” (What Happens To The Brain In Alzheimer’s Disease?). The tau tangles and amyloid plaques together play a huge role in synapse reduction and neuronal death in an Alzheimer’s patient, progressively growing and further destroying cognitive functions.

 

SYMPTOMS & EFFECTS

Alzheimer’s Disease affects the neurological aspects of a person, often resulting in a decline in logical, behavioral, and social skills. All patients of the disease end up with dementia, which is basically the umbrella term for the loss of cognitive functions. The symptoms of the disease usually are spotted after the age of 65, which make it hard for scientists to truly dive into the matter. Since most symptoms don’t show up regularly at a younger age, many people don’t realize they have Alzheimer’s until the effects are damaging. Nonetheless, these are some of the symptoms of having Alzheimer’s (10 Signs And Symptoms of Alzheimer’s):

  • “Memory Loss That Disrupts Daily Life”

  • “Challenges In Planning Or Solving Problem”

  • “Difficulty Completing Familiar Tasks”

  • “Confusion With Time Or Place”

  • “Trouble Understanding Visual And Spatial Relationships”

  • “New Problems With Words In Speaking Or Writing”

  • “Misplacing Things And Losing The Ability To Retrace Steps”

  • “Decreased Or Poor Judgement”

  • “Withdrawal From Work Or Social Activities”

  • “Changes In Mood And Personality”

As humans, we have to realize the severity of this condition. They can start wandering around in open places, or forget what they ate for breakfast. In severe situations, our loved ones can reach a point where they cannot perform tasks that we don’t even hesitate to think about. It can reach the point where they need help to put on their clothes the correct way. This disease is not something that is easy to research on, but one that truly deserves all the attention, especially with its severity.

 

TREATMENTS

Even while scientists and researchers have spent much time and effort trying to understand Alzheimer’s, unfortunately, no cure has been discovered. However, there are many medications and drugs that can aid in the presence of the symptoms, such as lesson memory loss.

All drugs approved by the FDA are targeted at two neurotransmitters: acetylcholine and glutamate. Acetylcholine is an organic chemical that plays a major role in neural communication and “influences synaptic transmission” (Picciotto, 2012). One example of a drug patients take is cholinesterase inhibitors. When a neuron releases the neurotransmitter acetylcholine, it binds to the acetylcholine receptors on the receiving neuron, allowing communication to happen between the two neurons. However, there is another enzyme involved in the communication, called acetylcholinesterase, which breaks down acetylcholine into its components, acetic acid and choline. Acetylcholinesterase is needed in this situation because it makes sure too much acetylcholine isn’t built up on the receptors, creating a sense of balance. Seems good so far, right? However, acetylcholine “is decreased in both concentration and function in patients with Alzheimer's disease” (Francias, 2005). This means that the neurons of patients with Alzheimer’s already lack acetylcholine, and having acetylcholinesterase to “eat away” at the few that they have doesn’t allow for much neural communication. Since acetylcholinesterase is a type of cholinesterase, researchers had the idea to give patients a cholinesterase inhibitor, which basically blocks the acetylcholinesterase from doing its job. Now, since the inhibitor is in the mix, the acetylcholinesterase is blocked, and more acetylcholine can connect to their receptors, allowing better neural communication. The side effects of cholinesterase inhibitors are mainly nausea, vomiting, diarrhea, and loss of appetite (Singh and Sadiq, 2020).

The second type of drug that Alzheimer’s patients are prescribed with, memantine, targets the neurotransmitter glutamate. Normally, glutamate is essential to help the brain with its learning and memory abilities. However, it is an excitatory neurotransmitter, implying that at high concentrations, the chemical is excitotoxic and can destroy the neuron (Newcomer et al., 2000). When glutamate is released from the transmitting neuron, it connects to the NMDA receptors on the receiving neuron. NMDA receptors are glutamate receptors, meaning they bind to glutamate molecules, but are also a protein channel for ions. In simpler terms, when a NMDA receptor is binded with glutamate, the channel opens up and allows ions to pass through into the neuron. In the case of a patient with Alzheimer’s, there is a high level of glutamate molecules, meaning that the NMDA channel is always open, allowing too many ions to pass into the neuron and destroy it, a term commonly known as “excitotoxicity” (Wang and Reddy, 2018). Therefore, doctors give Alzheimer’s patients memantine, which blocks the glutamate receptors on NMDA, making sure that the channel doesn’t open up as much and too many ions don’t pass through. As a result, the neurons don’t die from excitotoxicity and synaptic plasticity is improved. Side effects include headaches, confusion and dizziness (Memantine).

 

CONCLUSION

Alzheimer’s Disease is definealty one topic that scientists and doctors are still trying to completely comprehend. The intense levels of biochemistry behind the illness are being studied in labs all around the world. Due to the lack of biotechnical inventions that may help detect the disease from an earlier age, many research studies are missing much information that are considered crucial to develop the perfect cure. However, there are still many ways that one may spot the symptoms of AD and treat its behavioral, social, and cognitive effects. Even while the journey of understanding Alzheimer’s Disease is still at its infancy, hopefully, there will come a day where we won’t have to worry when our loved ones are facing difficulties because of neurodegenerative diseases.



 

Work Cited


“Alzheimer's Disease.” Mayo Clinic, Mayo Foundation for Medical Education and Research,


Nicolas, Maya, and Bassem A. Hassan. “Amyloid Precursor Protein and Neural

Development.” Development, Oxford University Press for The Company of Biologists


Rajasekhar, K., Chakrabarti, M., Govindaraju, T. “Function and Toxicity of Amyloid Beta and

Recent Therapeutic Interventions Targeting Amyloid Beta in Alzheimer's Disease.”

Chemical Communications, The Royal Society of Chemistry, 31 July 2015,


Loo, D. T., et al. “Apoptosis Is Induced by Beta-Amyloid in Cultured Central Nervous System

Neurons.” Proceedings of the National Academy of Sciences of the United States of

America, U.S. National Library of Medicine, 1 Sept. 1993,


Avila, Jesus, et al. “Tau Structures.” Frontiers in Aging Neuroscience, Frontiers Media S.A., 8


Iqbal, K., et al. “Tau in Alzheimer Disease and Related Tauopathies.” Current Alzheimer

Research, U.S. National Library of Medicine, Dec. 2010,


“What Happens to the Brain in Alzheimer's Disease?” National Institute on Aging, U.S.

Department of Health and Human Services, 16 May 2017, www.nia.nih.gov/health/what-


“10 Early Signs and Symptoms of Alzheimer's.” Alzheimer's Disease and Dementia,

Alzheimer's Association, www.alz.org/alzheimers-dementia/10_signs.


Picciotto, Marina R, et al. “Acetylcholine as a Neuromodulator: Cholinergic Signaling Shapes

Nervous System Function and Behavior.” Neuron, U.S. National Library of Medicine, 4


Francis, Paul T. “The Interplay of Neurotransmitters in Alzheimer's Disease: CNS Spectrums.”

Cambridge Core, Cambridge University Press, 7 Nov. 2014,


Singh, Ravneet, and Nazia M. Sadiq. “Cholinesterase Inhibitors.” StatPearls, U.S. National

Library of Medicine, 16 May 2020, www.ncbi.nlm.nih.gov/books/NBK544336/.


Newcomer, J W, et al. “NMDA Receptor Function, Memory, and Brain Aging.” Dialogues in

Clinical Neuroscience, Les Laboratoires Servier, Sept. 2000,


Wang, Rui, and P Hemachandra Reddy. “Role of Glutamate and NMDA Receptors in

Alzheimer's Disease.” Journal of Alzheimer's Disease : JAD, U.S. National Library of


“Memantine (Oral Route) Side Effects.” Mayo Clinic, Mayo Foundation for Medical

Education and Research, 1 Feb. 2020, www.mayoclinic.org/drugs-

Comments

bottom of page