With the constant evolution of science and medicine, people are living longer than ever before, though an aging population comes with many new challenges. One illness with poor patient outcomes is Alzheimer's, marked by worsening dementia that causes memory loss, personality changes, and trouble with higher functioning. Emerging research shows that prion diseases and non-infectious neurodegenerative diseases may be more similar than previously thought, consequently uncovering new possible treatment routes for progressive and irreversible diseases of the brain.
Diseases that are neurodegenerative, such as Alzheimer's, have a similar mechanism to prion diseases that infect the brain and slowly destroy it (Frost and Diamond, 2010). The mechanism …show more content…
Similarly, the progression of Alzheimer's disease was investigated in various pathological studies that concluded the disease begins in the trans-entorhinal region of the brain, begins to degenerate the entorhinal cortex, soon after progressing to the hippocampus, amygdala, and neocortex (Frost and Diamond, 2010). Consequently, the deterioration of the amygdala leads to the emotional dysfunction seen in Alzheimer's patients, while the hippocampal destruction leads to memory loss, resulting in two of the most debilitating symptoms of the disease. Based on the pattern of disease progression, it is believed that PrPSc spreads through neuronal networks (Frost and Diamond, 2010), converting healthy cells to the diseased type as they come in contact. Knowing how this degenerative disease spreads through the brain, and the similarities with prion diseases, has important implications for future treatments that may help stop or slow the progression of Alzheimer's. One emerging area of research involves finding therapeutic strategies to stop the spread of the PrPSc protein, perhaps using stem cells, antibodies, or transplanted cells resistant to the misfolded protein (Frost and Diamond, …show more content…
The results revealed similar atrophy patterns in the diseased patients, in addition to the spread of Alzheimer's following a prion-like propagation (Raj, Kuceyeski, and Weiner, 2012), also similar to findings from Frost and Diamond (2010). The patterns lead the researches to conclude that Alzheimer's disease is spread through the brain's connectivity network in a predictable fashion, and was not spread randomly by proximity (Raj, Kuceyeski, and Weiner,
Diseases that are neurodegenerative, such as Alzheimer's, have a similar mechanism to prion diseases that infect the brain and slowly destroy it (Frost and Diamond, 2010). The mechanism …show more content…
Similarly, the progression of Alzheimer's disease was investigated in various pathological studies that concluded the disease begins in the trans-entorhinal region of the brain, begins to degenerate the entorhinal cortex, soon after progressing to the hippocampus, amygdala, and neocortex (Frost and Diamond, 2010). Consequently, the deterioration of the amygdala leads to the emotional dysfunction seen in Alzheimer's patients, while the hippocampal destruction leads to memory loss, resulting in two of the most debilitating symptoms of the disease. Based on the pattern of disease progression, it is believed that PrPSc spreads through neuronal networks (Frost and Diamond, 2010), converting healthy cells to the diseased type as they come in contact. Knowing how this degenerative disease spreads through the brain, and the similarities with prion diseases, has important implications for future treatments that may help stop or slow the progression of Alzheimer's. One emerging area of research involves finding therapeutic strategies to stop the spread of the PrPSc protein, perhaps using stem cells, antibodies, or transplanted cells resistant to the misfolded protein (Frost and Diamond, …show more content…
The results revealed similar atrophy patterns in the diseased patients, in addition to the spread of Alzheimer's following a prion-like propagation (Raj, Kuceyeski, and Weiner, 2012), also similar to findings from Frost and Diamond (2010). The patterns lead the researches to conclude that Alzheimer's disease is spread through the brain's connectivity network in a predictable fashion, and was not spread randomly by proximity (Raj, Kuceyeski, and Weiner,