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Alzheimer’s disease offers clues to fighting brain cancer
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This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Glioma is the most common and lethal form of brain cancer. Among patients with the highest grade of glioma, fewer than 6% survive up to 5 years after diagnosis. Interestingly, glioma is extremely rare in one large population of patients patients with Alzheimer’s disease. That suggests that an anti-glioma molecule could play a critical role in the development of Alzheimer’s. In a recent study, researchers assessed one possible candidate: presenilin-1. Presenilin-1 is a protein that assists the formation of amyloid beta, the main component of the hallmark plaques found in the brains of patients with Alzheimer’s. Experiments showed that high presenilin-1 levels in glioma tissue from patients correlated with low tumor proliferation. Closer examination revealed that presenilin-1 kept cancer from spreading by preventing tumor cells from replicating their DNA. This mechanism could explain the poor prognosis of glioma patients with low levels of presenilin-1..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

Subject:
Biology
Life Science
Material Type:
Diagram/Illustration
Reading
Provider:
Research Square
Provider Set:
Video Bytes
Date Added:
04/24/2020
Baicalein inhibits heparin-induced Tau aggregation by initializing Tau oligomer formation
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This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Alzheimer’s disease (AD) is the leading cause of dementia in the aged population. The key feature of AD is the deposition of two different kinds of protein aggregates in the brain, and at the point of aggregate formation, treatment becomes difficult. A recent study focused on how to prevent the aggregation of one protein: the microtubule-associated protein Tau, which forms neurofibrillary tangles. Following up on research indicating that polyphenolic compounds can serve as neuroprotective agents, researchers analyzed the ability of the polyphenol Baicalein to inhibit the aggregation of Tau. In vitro, Baicalein blocked Tau aggregation and paired helical filament dissolution via an oligomer capture and dissociation mechanism. It also dissolved preformed mature fibrils of Tau, creating Tau oligomers, with no effect on the viability of neuronal cells..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

Subject:
Biology
Life Science
Material Type:
Diagram/Illustration
Reading
Provider:
Research Square
Provider Set:
Video Bytes
Date Added:
02/26/2021
Cognitive Neuroscience of Remembering: Creating and Controlling Memory
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This course is offered during the Independent Activities Period (IAP), which is a special 4-week term at MIT that runs from the first week of January until the end of the month.
This survey course is intended to review memory and its impact on our lives. Memories make us who we are, and make us what we are going to become. The loss of memory in amnesia can cause us to lose ourselves.
Memory provides a bridge between past and present. Through memory, past sensations, feelings, and ideas that have dropped from conscious awareness can be subsequently recovered to guide current thought and action. In this manner, memory allows us to locate our car in the parking lot at the end of the day or guides us to avoid retelling the same joke to the same friend. This seminar will focus on how memories are created and controlled such that we are able to remember the past. Recent insights from non-human electrophysiological and human brain imaging research will be emphasized.

Subject:
Biology
Life Science
Physical Science
Material Type:
Full Course
Provider:
MIT
Provider Set:
MIT OpenCourseWare
Author:
Wagner, Anthony
Date Added:
01/01/2002
Cozied up cell parts help flies with Alzheimer’s-like symptoms live longer
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This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Alzheimer’s disease is a progressive brain disorder that gradually destroys memory and thinking skills Every year, the number of people affected by the disease continues to grow That has some researchers looking to the fruit fly for answers One team has found that linking two parts of the cell closer together may help Linking the endoplasmic reticulum, which forms proteins and stores calcium to the mitochondria, which power the cell can actually improve motor function in fruit flies and help them live longer This technique works in flies with brain plaques similar to those found in humans with Alzheimer’s disease Part of the reason could be improved access to calcium Forcing the organelles together helps calcium migrate more easily from the endoplasmic reticulum to the mitochondria This sends the mitochondria into overdrive because calcium acts as a lubricant for the mitochondrial machinery that pumps out energy So easy access to calcium means more energy output Clarifying how that transl.."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

Subject:
Applied Science
Health, Medicine and Nursing
Material Type:
Diagram/Illustration
Reading
Provider:
Research Square
Provider Set:
Video Bytes
Date Added:
12/23/2019
PP1γ links neuronal insulin resistance and Alzheimer’s-like pathology in vitro
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This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Insulin resistance in neurons is linked to neurodegenerative diseases like Alzheimer’s disease and Parkinson’s disease. The regulation of neuronal insulin signaling by phosphatases isn’t fully understood. To learn more, researchers recently investigated the role of the protein phosphatase PP1 in neuronal insulin signaling and resistance. They found that the PP1 isoform PP1γ, but not PP1α, participated in insulin signaling in mouse and human neuroblastoma cell lines. PP1γ dephosphorylated AKT2, thereby limiting AS160 phosphorylation, GLUT4 translocation, and glucose uptake. It also regulated GSK3β phosphorylation through AKT2, while it regulated GSK3α phosphorylation through IKK and MLK3. Through its effects on these two GSK3 isoforms, PP1γ fine-tuned the development of Aβ plaques and neurofibrillary tangles these are hallmarks of Alzheimer’s disease. Specifically, PP1γ increased neurofibrillary tangle formation but suppressed amyloid β plaque formation in neuronal cells..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

Subject:
Biology
Life Science
Material Type:
Diagram/Illustration
Reading
Provider:
Research Square
Provider Set:
Video Bytes
Date Added:
05/01/2023
Unraveling the genetic risk factors for Alzheimer’s disease
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This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"The strongest genetic risk factor for Alzheimer’s disease may impair the body’s cellular recycling system, allowing the build-up of harmful byproducts in the brain. People carrying the gene variant known as APOE4 are at an increased risk for the early development of Alzheimer’s and show high numbers of the brain plaques characteristic of the disease. But the underlying reason for this effect isn’t clear. Now, researchers have shown that APOE4 interferes with autophagy -- the body’s way of recycling unneeded or harmful cellular material – providing new insights into how and why APOE4 conveys such a strong risk for Alzheimer’s. The team looked at the relationship between APOE4 and a protein known as TFEB, considered a master regulator of autophagy-related genes. Prior studies have linked reduced TFEB expression to the presence of amyloid-beta plaques in the brain..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

Subject:
Applied Science
Health, Medicine and Nursing
Material Type:
Diagram/Illustration
Reading
Provider:
Research Square
Provider Set:
Video Bytes
Date Added:
09/20/2019
A new perspective on the role of phosphorylation in Alzheimer’s and other tau pathologies
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This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Normally bound to the microtubules that give neurons their structure, the protein tau becomes detached in the brains of patients with Alzheimer’s disease. That leads to the fibrillary tangles that have become the hallmark of the disease. Most textbooks explain that post-translational modifications, or PTMs, in the form of excessive phosphorylation trigger the formation and growth of these bundles. But new findings propose a subtle though crucial refinement. Researchers from the Brain Mind Institute at the EPFL in Switzerland have discovered that while phosphorylation does trigger tau detachment, it doesn’t appear to promote tangle growth. It actually protects against it. Their findings offer a new perspective on the role of phosphorylation in tau pathologies, while encouraging the design of therapeutics that target tau detachment. Numerous studies have homed in on hyperphosphorylation as a trigger for tau pathologies. Unfortunately, they’ve done so with relatively poor resolution..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

Subject:
Applied Science
Health, Medicine and Nursing
Material Type:
Diagram/Illustration
Reading
Provider:
Research Square
Provider Set:
Video Bytes
Date Added:
02/14/2020