The Search for A Cure: Alzheimer's
Alzheimer's disease is one of the most common causes of dementia, which is a name for general memory loss. Alzheimer's is a disease that is common amongst aging adults and especially for those who are genetically inclined to develop It. In the early stages of Alzheimer's, the disease destroys neurons and the associated neuronal connections and in the later stages of Alzheimer's the disease forms in brain regions associated with memory. Then in the later stages of the disease plaques form around brain structures associated with learning and memory while tangles form inside of neurons interfering with machinery eventually resulting in neuronal death. There are currently no known cures for Alzheimer's disease, but recent discoveries have opened the doors to new treatments. In the article "Induced Adult Neurogenesis plus BDNF Mimics the Effects of Exercise on Cognition in an Alzheimer's Mouse Model" by Se Hoon Choi and the article "Serum pro-BDNF levels correlate with phospho-tau staining in Alzheimer's disease" by Krishna Bharani both researchers explore the Brain-derived neurotropic factor and its linkage to Alzheimer's disease.
In Krishna Bharani's article "Serum pro-BDNF levels correlate with phospho-tau staining in Alzheimer's disease" he and other researchers explore the correlation between different types of BDNF and their corresponding with levels within the human brain that they studied in samples that were taken post-mortem. "total BDNF, precursor BDNF (pro-BDNF), and mature BDNF were measured in cerebrospinal fluid, serum, and 3 postmortem brain regions. Histological markers for AD pathology, the BDNF cognate receptor (TrkB), and glia were measured in the hippocampus…" (Bharani et al., 2019) The researchers used these markers to compare what levels of each type of BDNF and their corresponding receptors were found in the hippocampal tissue. They found that there were high amounts of serum pro-BDNF with the staining of amyloid plaques in Alzheimer's brains which is a known trait of Alzheimer's brains. Most importantly, the researchers found that there were low amounts of pro-BDNF levels in the hippocampus and other cortices of the brain. There were also lower pro-BDNF levels observed in the entorhinal and frontal cortices in Alzheimer's brains when compared with controls as well as low TrkB receptors found in the hippocampus. These results demonstrate that there is an inverse relationship between the BDNF and Alzheimer's disease which shows that there is good reason to believe there is potential for developing therapy through the BDNF pathway.
In "Induced Adult Neurogenesis plus BDNF Mimics the Effects of Exercise on Cognition in an Alzheimer's Mouse Model" by Se Hoon Choi and others, the research looked into the relationships between adult hippocampal neurogenesis (AHN), exercise, BDNF, and Alzheimer's disease (AD). The researchers first began their research because of the result that they found when having AD mice exercise. They found that when AD (Alzheimer's disease) mice would exercise they were inducing AHN and elevating their levels of BDNF. By doing all three they were able to ameliorate cognition in AD mice. The researchers "successfully mimicked the beneficial effects of exercise on AD mice by genetically and pharmacologically inducing AHN in combination with elevating BDNF levels" (Choi et al., 2018). These results are very promising because they provide further concrete insight into the development of a new treatment for Alzheimer's disease.
Both research studies contribute highly to the development of a treatment for AD. Soon researchers will finally be able to more effectively slow the degeneration of memory in people with AD if such treatment is developed.
In Krishna Bharani's article "Serum pro-BDNF levels correlate with phospho-tau staining in Alzheimer's disease" he and other researchers explore the correlation between different types of BDNF and their corresponding with levels within the human brain that they studied in samples that were taken post-mortem. "total BDNF, precursor BDNF (pro-BDNF), and mature BDNF were measured in cerebrospinal fluid, serum, and 3 postmortem brain regions. Histological markers for AD pathology, the BDNF cognate receptor (TrkB), and glia were measured in the hippocampus…" (Bharani et al., 2019) The researchers used these markers to compare what levels of each type of BDNF and their corresponding receptors were found in the hippocampal tissue. They found that there were high amounts of serum pro-BDNF with the staining of amyloid plaques in Alzheimer's brains which is a known trait of Alzheimer's brains. Most importantly, the researchers found that there were low amounts of pro-BDNF levels in the hippocampus and other cortices of the brain. There were also lower pro-BDNF levels observed in the entorhinal and frontal cortices in Alzheimer's brains when compared with controls as well as low TrkB receptors found in the hippocampus. These results demonstrate that there is an inverse relationship between the BDNF and Alzheimer's disease which shows that there is good reason to believe there is potential for developing therapy through the BDNF pathway.
In "Induced Adult Neurogenesis plus BDNF Mimics the Effects of Exercise on Cognition in an Alzheimer's Mouse Model" by Se Hoon Choi and others, the research looked into the relationships between adult hippocampal neurogenesis (AHN), exercise, BDNF, and Alzheimer's disease (AD). The researchers first began their research because of the result that they found when having AD mice exercise. They found that when AD (Alzheimer's disease) mice would exercise they were inducing AHN and elevating their levels of BDNF. By doing all three they were able to ameliorate cognition in AD mice. The researchers "successfully mimicked the beneficial effects of exercise on AD mice by genetically and pharmacologically inducing AHN in combination with elevating BDNF levels" (Choi et al., 2018). These results are very promising because they provide further concrete insight into the development of a new treatment for Alzheimer's disease.
Both research studies contribute highly to the development of a treatment for AD. Soon researchers will finally be able to more effectively slow the degeneration of memory in people with AD if such treatment is developed.
References:
Choi, S., Bylykbashi, E., Chatila, Z., Lee, S., Pulli, B., Clemenson, G., Kim, E., Rompala, A., Oram, M., Asselin, C., Aronson, J., Zhang, C., Miller, S., Lesinski, A., Chen, J., Kim, D., van Praag, H., Spiegelman, B., Gage, F. and Tanzi, R., 2018. Combined adult neurogenesis and BDNF mimic exercise effects on cognition in an Alzheimer’s mouse model. Science, 361(6406), p.eaan8821.
Bharani, Krishna L., et al. “Serum pro-BDNF Levels Correlate with Phospho-Tau Staining in Alzheimer's Disease.” Neurobiology of Aging, vol. 87, 2020, pp. 49–59., doi:10.1016/j.neurobiolaging.2019.11.010.
Choi, S., Bylykbashi, E., Chatila, Z., Lee, S., Pulli, B., Clemenson, G., Kim, E., Rompala, A., Oram, M., Asselin, C., Aronson, J., Zhang, C., Miller, S., Lesinski, A., Chen, J., Kim, D., van Praag, H., Spiegelman, B., Gage, F. and Tanzi, R., 2018. Combined adult neurogenesis and BDNF mimic exercise effects on cognition in an Alzheimer’s mouse model. Science, 361(6406), p.eaan8821.
Bharani, Krishna L., et al. “Serum pro-BDNF Levels Correlate with Phospho-Tau Staining in Alzheimer's Disease.” Neurobiology of Aging, vol. 87, 2020, pp. 49–59., doi:10.1016/j.neurobiolaging.2019.11.010.
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