Understanding Alzheimer's: What Happens in the Brain ?? Part 2 - The Neurology-Nutrition Series
Dear readers,
A healthy mind creates a healthy body and vice versa. To ensure overall vitality, brain health is key. In this quick post of Heal Thyself, I want to share the background biology of Alzheimer's Disease.
Alzheimer's disease is a complex neurodegenerative disorder characterized by progressive cognitive decline, memory loss, and changes in behavior and personality.
In my second year of college, I was very fortunate to do a project centered around Alzheimer's and holistic rehabilitation for all the stakeholders affected.
Since the behind-the-scenes, are not very well known, here is a quick overview of what really progresses and takes place in the brain in the case of Alzheimer's.
(At the end of this post, find a quick list of things you can do to minimize your risk of this neurodegenerative disorder.)
First case scenario:
Amyloid Beta (Aβ) Plaque Formation
Alzheimer's is mostly associated with the accumulation of abnormal protein aggregates in the brain, particularly amyloid beta (Aβ) plaques. These plaques are formed from the misfolding and aggregation of amyloid precursor protein (APP), leading to the production of a toxin called Aβ peptides.
The accumulation of these Aβ plaques disrupts normal brain cell functions and communication, leading to injury of the cells and death. Aβ peptides are thought to impair synaptic function, ie., it interferes with neurotransmitter signaling, and trigger inflammatory responses in the brain. Over time, the accumulation of Aβ plaques contributes to widespread neuronal dysfunction and loss, particularly in regions of the brain involved in learning and memory, such as the hippocampus and cortex.
Second case:
Tau Protein Hyperphosphorylation and Neurofibrillary Tangle Formation
In addition to Aβ plaques, Alzheimer's disease is characterized by the abnormal phosphorylation and aggregation of tau protein, leading to the formation of neurofibrillary tangles (NFTs) within neurons. Tau protein is normally involved in stabilizing microtubules and supporting neuronal structure and function. However, in Alzheimer's disease, tau becomes hyperphosphorylated, causing it to detach from microtubules and form insoluble aggregates.
The formation of neurofibrillary tangles disrupts intracellular transport mechanisms, impairs communication, and ultimately leads to neuronal dysfunction and death. NFTs are particularly abundant in the hippocampus and other brain regions critical for memory and cognition. The presence of NFTs correlates closely with cognitive decline and disease progression in Alzheimer's disease.
Third case scenario:
Neuroinflammation and Oxidative Stress
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Neuroinflammation and oxidative stress are prominent features of Alzheimer's disease pathology. In response to the accumulation of Aβ plaques and NFTs, microglial cells and astrocytes in the brain become activated and release pro-inflammatory cytokines, chemokines, and reactive oxygen species (ROS).
Chronic inflammation of the brain and oxidative stress contribute to neuronal damage and death, exacerbating the progression of Alzheimer's disease. Inflammatory mediators disrupt synaptic function, impair neurogenesis, and promote the production of toxic Aβ peptides.
Oxidative stress further damages cellular components, including proteins, lipids, and DNA, leading to mitochondrial dysfunction and neuronal apoptosis. Additionally, neuroinflammation contributes to blood-brain barrier dysfunction, allowing peripheral immune cells to infiltrate the brain and exacerbate neurodegeneration.
What you can do to minimize the risk of Alzheimer's
For more details, please visit my website: shevauneuron.wordpress.com
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Citations
Fig 1: Kuragano, M., Yamashita, R., Chikai, Y. et al. Three-dimensional real time imaging of amyloid β aggregation on living cells. Sci Rep 10, 9742 (2020). https://doi.org/10.1038/s41598-020-66129-z
Fig 2: Eshraghi, Mehdi & Adlimoghaddam, Aida & Mahmoodzadeh, Amir & Sharifzad, Farzaneh & Yasavoli, Hamed & Lorzadeh, Shahrokh & Albensi, Benedict & Ghavami, Saeid. (2021). Alzheimer’s Disease Pathogenesis: Role of Autophagy and Mitophagy Focusing in Microglia. International Journal of Molecular Sciences. 22. 3330. 10.3390/ijms22073330.
Fig 3: Gorelova, A., & Trentrock, A. (2021, August 26). Brain tissue inflammation drives Alzheimer’s disease. University of Pittsburgh Medical Center. Retrieved from https://www.upmc.com/media/news/082621-pascoal-alzheimer