Brandeis’s Students to End Alzheimer’s Disease (SEAD) discussed the basics of Alzheimer’s disease in a lecture on Thursday. The event, titled the “Alz Talk,” featured Dr. Jonathan Jackson — Research Fellow in Neurology at Harvard Medical School — who spoke about the disease and presented recent developments in the field.

Jackson began his talk by explaining how normal, healthy, human memory works. He dispelled the notion that memory is like a “video camera,” which captures information and then replays it as requested. Instead, he suggested that a better metaphor for memory is a Lego block. According to Jackson, “if you think of memory as a reconstructive Lego-like process, then as you rebuild memories [each time] they are likely to change slightly.” Additionally, he used this metaphor to point out that “memories are inherently fallible because they are malleable.”

He then explained that this reconstructive memory process primarily occurs in a central part of the brain called the medial temporal lobe. As adults get older, their brain volume gradually declines, but this decline is not uniform throughout brain regions, he noted. In fact, Jackson said, “the region of the brain that is most sensitive to age-related decline is the [medial temporal lobe] … and this is why as individuals get older … they have memory problems.” However, he emphasized that this decline is an entirely normal part of the aging process and posed the question: “If this is normal, how [do] we differentiate it from Alzheimer’s disease?”

Jackson defined the disease process of Alzheimer’s as having two major parts: a peptide called Amyloid and a protein called Tau. Jackson began by describing Amyloid, arguing that is like plastic wrap. He said that in the brain, the Amyloid peptide is supposed to be “cleaved” in a certain way; however, in Alzheimer’s patients, the cleaving process goes wrong, leaving people with “this sticky gunk that sticks only to itself, and it’s useless to you” — much like poorly torn off plastic wrap. Then, Jackson explained, these “messed-up pieces of Amyloid” congregate and form Amyloid plaques which “short-circuit” brain cells.

He added that up until just a few years ago, researchers believed that Amyloid was solely responsible for Alzheimer’s. However, he noted, it is now known that Tau is also necessary for the disease to develop. Jackson defined Tau as “a protein in the brain that is really involved in maintaining the cell structures, and when Alzheimer’s strikes, this Tau protein essentially becomes poison … and essentially weakens the brain cell from the inside.” Jackson summed up the disease by saying, “You’ve got this one-two punch for each brain cell, so Tau is weakening the brain cell from the inside while Amyloid is attacking from the outside.”

Just like normal aging, Alzheimer’s disease does not affect the brain uniformly, but it first attacks the brain cells in the medial temporal lobe and, as Jackson asserted, “this is why Alzheimer’s disease affects memory — because it attacks [that] part of the brain.” However, due to brain scans that can detect Amyloid buildup in the brain, normal aging and Alzheimer’s are easily distinguishable, he said. In fact, Jackson revealed that brain scans conducted twenty-five years before the diagnosis of Alzheimers are “able to see this disease process in action.” Jackson told the audience that he believes these scans are allowing researchers to focus on the “actual disease process” instead of just the symptom of memory loss.

Finally, Jackson addressed several recent developments in Alzheimer’s treatments. The first study he discussed involves scanning ultrasound technology, a technique which came “out of left-field” for the Alzheimer’s community as it is a non-pharmacological approach. Jackson described this approach as using common ultrasounds to “open” the blood-brain barrier. This would allow for lysosomes, specialized parts of cells, to enter the brain. These lysosomes then break down the Amyloid build-up and clear it out, leading to significant memory restoration and improvement. Despite the seemingly optimistic findings, Jackson cautioned that using ultrasounds to treat Alzheimer’s has only “been tested on ten rats” and that there still needs to be “lots more research” on this technique before it can be used on humans.

Jackson also spoke of how following MIND — Mediterranean-Intervention for Neurodegenerative Delay — diets could lower the risk of Alzheimer’s disease. He stated that not only did following such a diet greatly reduce the chance of an individual developing Alzheimer’s, but just “moderately adhering” to the diet reduced the risk of Alzheimer’s as well. Jackson described these findings as “the feel-good story of 2015.”

A brief question-and-answer session followed Jackson’s talk. Several audience members asked Jackson to elaborate on the different scientific findings he mentioned in his lecture. Jackson ended the event by expressing his hope that “no one in [this] generation will have to worry about getting Alzheimer’s.”