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2-Minute Neuroscience: Alzheimer's Disease
- Subjects: Neurosciences
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- neurodegenerative disease
- Alzheimer's
- AD
- tau protein
- acetylcholinesterase
Video Introduction
The content is sourced from: https://youtu.be/I6K10aif0tE
Alzheimer's disease is the most common form of neurodegenerative disease. In addition to the widespread neurodegeneration that occurs in Alzheimer's disease, there are specific neurobiological abnormalities that appear in the brains of Alzheimer's patients. For example, clusters of a misfolded form of a protein called amyloid beta develop around neurons; the clusters are called amyloid plaques. Additionally, clusters of misfolded tau protein develop inside neurons; these clusters are called neurofibrillary tangles. The most common treatments for Alzheimer's disease are acetylcholinesterase inhibitors, which are drugs that inhibit the breakdown of the neurotransmitter acetylcholine. Acetylcholine is thought to be important to healthy cognition, but acetylcholinesterase inhibitors have relatively modest effects on the symptoms of Alzheimer's disease. [1]
TRANSCRIPT:
Welcome to 2 minute neuroscience, where I simplistically explain neuroscience topics in 2 minutes or less. In this installment I will discuss Alzheimer’s disease.
Alzheimer’s disease is the most common form of neurodegenerative disease, meaning it is characterized by the degeneration and death of neurons. It is classified as a type of dementia, a term that refers to a category of brain disorders that involve memory loss and cognitive impairment. Alzheimer’s most often affects adults over the age of 65. The causes of the disease are not well understood and genetics and environmental factors are thought to be involved. Alzheimer’s disease is associated with neuronal death throughout the brain, which can be extensive enough that regions of the brain appear atrophied (or shrunken) compared to a healthy brain.
A hallmark sign of Alzheimer’s disease is the formation of clusters of misfolded proteins both inside and outside of neurons. One of these proteins, amyloid beta protein, is found in the extracellular space around neurons in a healthy brain. During Alzheimer’s, however, misfolded forms of amyloid beta clump together in deposits called amyloid plaques. Another protein called tau protein, which is normally found inside neurons and involved in maintaining neuronal structure, is also found in a misfolded state in Alzheimer’s. It accumulates inside neurons in bundles called neurofibrillary tangles. Although amyloid plaques and neurofibrillary tangles are hallmark signs of Alzheimer’s disease, it is unclear if they contribute to neurodegeneration or are part of the brain’s response to it.
The most common treatments for Alzheimer’s disease involve drugs that inhibit the activity of acetylcholinesterase, an enzyme that breaks down the neurotransmitter acetylcholine. The drugs, called acetylcholinesterase inhibitors, increase levels of acetylcholine, which is thought to promote healthy cognition and memory. The effects of these treatments are modest, however, and they do not stop neurodegeneration in Alzheimer's; thus, they are not a cure for the disease.
References
- Purves D, Augustine GJ, Fitzpatrick D, Hall WC, Lamantia AS, McNamara JO, White LE. Neuroscience. 4th ed. Sunderland, MA. Sinauer Associates; 2008.
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Challenged, N. 2-Minute Neuroscience: Alzheimer's Disease. Encyclopedia. Available online: https://encyclopedia.pub/video/video_detail/1194 (accessed on 15 November 2024).
Challenged N. 2-Minute Neuroscience: Alzheimer's Disease. Encyclopedia. Available at: https://encyclopedia.pub/video/video_detail/1194. Accessed November 15, 2024.
Challenged, Neuroscientifically. "2-Minute Neuroscience: Alzheimer's Disease" Encyclopedia, https://encyclopedia.pub/video/video_detail/1194 (accessed November 15, 2024).
Challenged, N. (2024, April 07). 2-Minute Neuroscience: Alzheimer's Disease. In Encyclopedia. https://encyclopedia.pub/video/video_detail/1194
Challenged, Neuroscientifically. "2-Minute Neuroscience: Alzheimer's Disease." Encyclopedia. Web. 07 April, 2024.
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