Week 2: My World and the Real World

Mar 16, 2020

It’s strange to study Alzheimer’s disease when we’re facing a crisis in the field of public health. And yet, I’ve been slowly progressing with my Senior Project’s independent research as well as engaging in plenty of new activities at home.

Last we left off, I was just beginning to explore the relationship between blood flow to the brain and the emergence of AD. I continued along this path this week by exploring a second disease I had described in my Senior Project proposal: cerebral hypoperfusion. I had discovered that Aß amyloid resulted in ischaemic damage, which restricted blood flow to the brain. I was soon realizing that cerebrovascular diseases may be risk factors for AD, and one such disease was cerebral hypoperfusion. This week I examined three different studies into the role of cerebral hypoperfusion in AD pathology.

  1. Seth Love and J. Scott Miners (2015)                                                        Love and Miners examined the factors contributing to hypoperfusion in AD. They first note that reduced blood flow is due to inadequate blood supply rather than reduced metabolic demand for blood. They then find that a major contributor to cerebral hypoperfusion is the vasoconstrictor endothelin-1 or EDN1.
  2. Hansson et al. (2018)                                                                              Hansson et al. finds that cerebral hypoperfusion is not associated with increased Aß amyloid in elderly humans. Even when blood flow was significantly reduced, there seemed to be no connection to the uptake of amyloid ß or tau.
  3. Austin et al. (2011)                                                                                      Here, Austin et al. looks at the role of hypoperfusion in the pathology of AD. In contrast to Hansson et al., they found that hypoperfusion was evident in disease manifestation and there is overlap between the regions of each disease. They did note, however, that it is unclear whether decreased blood flow in AD was a cause or a result of disrupted hypoperfusion.

I looked at these findings a bit perplexed. There seemed to be some dispute over whether hypoperfusion played an important role in pathology. This proved to be quite a complex topic and I’ll need to explore in future weeks.

It’s hard to write about my independent research without also using this platform to reflect on the health crisis we are currently facing. I am not quite sure if I’ll ever be able to step foot at GWU Hospital for my on-site research only because of the corona cases that are slowly building up over these past two weeks. So with the time that I’ve had at home, I have been spending more time with my family watching Better Call Saul on Netflix and practicing some cooking. My brother, who just arrived this week from London and has self-quarantined himself in his room for 14 days. While I love the research I’m doing, I feel like I’m stuck in a bubble when I write these blog posts because there is so much happening outside of this project alone that I have had to focus on.



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