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.

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:

"There may be a silver lining for those at high risk for Alzheimer’s: as the chance of getting the disease goes up, certain treatments may become more effective. The risk of developing Alzheimer’s largely relies on a gene called APOE, with different variants conferring more or less risk. Usually, having a high-risk allele is bad news, but a group of researchers from New York University has reported that carrying the high-risk allele could actually boost responsiveness to immunotherapy, a promising new treatment option. The APOE gene helps determine how much beta-amyloid accumulates in the brain. Beta-amyloid starts as small misfolded bits of protein that clump together to form the plaques that are the hallmark of Alzheimer’s. As the plaques appear, the brain deteriorates, particularly in regions associated with memory. One way to potentially halt this process is to use antibodies that recognize beta-amyloid. The antibodies bind to the protein and signal to the immune system to clear it out..."

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

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.

Biology is designed for multi-semester biology courses for science majors. It is grounded on an evolutionary basis and includes exciting features that highlight careers in the biological sciences and everyday applications of the concepts at hand. To meet the needs of today’s instructors and students, some content has been strategically condensed while maintaining the overall scope and coverage of traditional texts for this course. Instructors can customize the book, adapting it to the approach that works best in their classroom. Biology also includes an innovative art program that incorporates critical thinking and clicker questions to help students understand—and apply—key concepts.

By the end of this section, you will be able to:Describe the symptoms, potential causes, and treatment of several examples of nervous system disorders

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:

"Once considered little more than “cell dust”, exosomes are receiving much deserved attention from the research community. Exosomes are tiny sacs whose job includes clearing the cell of certain lipids, proteins, and nucleic acids. But researchers are learning that exosomes are also crucial to signaling and communication between cells. A new review explores various ways exosomes help coordinate the metabolism of lipids in the body. Some of the most promising research describes what happens when exosomes’ ability to synthesize, transport, and degrade lipids is compromised. In some cases, that can lead to disorders such as atherosclerosis, cancer, obesity, and Alzheimer’s disease. Understanding how exosomes orchestrate metabolic activities could clue researchers in on new ways to diagnose and treat related diseases..."

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

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:

"Most genetic studies of Alzheimer’s disease compare patient DNA to controls to identify mutations that increase disease risk. That approach has identified some risk variants, but none have led to effective treatments, and most of the genetic contributors are still unknown. Now, a team of researchers is tackling the problem from the opposite side, asking why some high-risk elderly people don’t have Alzheimer’s – a strategy that has discovered a protective mutation in a gene that may be a good drug target. To find protective mutations for Alzheimer’s, the scientists first searched the Utah Population Database for families with above-average rates of Alzheimer's that also had at least four people who were resilient to the disease -- that is, they were cognitively normal, despite being 75 years old or older, and having the APOE e4 allele, which increases risk more than 5-fold per copy..."

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

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 associated with the misfolding of two major proteins, causing the accumulation of toxic protein aggregates. Amyloid-β aggregates extracellularly, forming plaques, and Tau aggregates intracellularly, forming neurofibrillary tangles. Post-translational modifications (PTMs) are important for the regulation of Tau’s function, but an imbalance in PTMs may lead to abnormal Tau function and aggregation. While methylation is an important PTM for Tau in its physiological state, the lysine methylation signature changes in Tau’s pathological form. These alterations may affect the intramolecular forces within the Tau molecule, resulting in altered conformations, and methylation can also interact with other PTMs, affecting Tau function and stability. Although more investigation is needed, it appears that in addition to post-translational methylation, DNA methylation also affects Tau regulation..."

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

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 and similar neurodegenerative diseases involve aggregation of the protein Tau and disruption of cell structural networks. The protein HDAC6 helps clear Tau aggregates and regulate the cytoskeleton, thus exerting neuroprotective effects. HDAC6’s catalytic domains mediate some of these functions, but the roles of another domain, the zinc finger ubiquitin-binding domain (ZnF UBP), are less understood. A recent study investigated the effects of purified HDAC6 ZnF UBP on cultured neuronal cells. The researchers found that HDAC6 ZnF UBP was nontoxic to cells, and cell imaging showed that it promoted reorganization of the cytoskeletal components actin and tubulin in ways that likely support neuron growth and migration. Localization of the protein ApoE in cell nuclei was increased, indicating improved neuronal health..."

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

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 affects 1 in 3 senior citizens worldwide. The hallmark of Alzheimer’s is the accumulation of abnormal protein deposits, including Tau and amyloid β, in neurons and glial cells in the brain. These deposits disrupt signal transduction by affecting lipid-based secondary messengers in the brain called phosphatidylinositols (PIs). PIs drive the reorganization of the cytoskeleton in glial cells, affecting many cellular processes. These dynamic molecules are tightly regulated by their phosphorylation status, which influences their abundance and localization. Because microglia in the brain must respond to chemotactic and pro-inflammatory signals, disrupting PIs alters microglial function, resulting in hyperactivation and inflammation. PI signaling typically drives actin remodeling to modulate phagocytosis, allowing glial cells to clear amyloid β aggregates and debris. Unfortunately, extensive amyloid β accumulation disrupts PI signaling, altering cytoskeleton regulation..."

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

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 and glioblastoma are the most common and devastating diseases in neurology and neurosurgery departments. In glioblastoma, the Alzheimer’s disease-related protein Presenilin1 limits cell proliferation by inhibiting the Wnt/β-catenin pathway. However, the function of this protein and the underlying mechanism are unclear. To learn more, researchers recently examined Presenilin1’s effects on glioblastoma in vitro and in vivo. Presenilin1 repressed glioblastoma cell migration, invasion, and mesenchymal transition in vitro. Interestingly, its expression was positively correlated with that of Sortilin, a pro-invasion molecule in glioma. Presenilin1 interacted with Sortilin at the transmembrane domain and inhibited its expression via cleavage, enabling β-catenin phosphorylation and repressing invasion in glioblastoma cells. In mouse subcutaneous and intracranial transplantation models, Presenilin1 stimulation dramatically reduced glioblastoma invasion and mesenchymal transition..."

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

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 human protein Tid-1 sits at the nexus of many key cellular processes and signaling pathways. These processes include cellular proliferation, growth, survival, aging, apoptosis, and even movement. Tid-1 is a member of the heat shock protein 40 family and helps other proteins fold correctly after translation or refold after a damaging stress event. Dysregulated Tid-1 behavior is involved in numerous human diseases including cancers, cardiomyopathies, and neurodegenerative disorders. Given its wide influence within the cell, Tid-1 could be a key biomarker or even therapeutic target for these diseases, but to leverage Tid-1 effectively, researchers need to understand its functionality in detail. To this end, a team of scientists consolidated the current research on human Tid-1. They found that Tid-1’s protein-protein interactions corresponded to its roles in various diseases and provide insight into how Tid-1 affects pathogenic developments..."

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

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:

"Diabetic encephalopathy (DE), a complication of type 2 diabetes (T2D), causes cognitive impairment that increases the chance of death. Because DE has no cure, investigating its mechanisms and finding new therapies are crucially important. DE has similar symptoms to Alzheimer's disease (AD), and both involve elevated β-amyloid peptide and hyperphosphorylated tau protein, so finding new therapies for DE could involve using what's already known about AD. The autophagy-lysosomal pathway (ALP) breaks down persistent proteins in cells and helps clear the neurofibrillary tangles and senile plaques characteristic of AD, and upstream genes called transcription factor EB (TFEB) and mechanistic target of rapamycin (mTOR) regulate ALP. Researchers used both cultured cells and a mouse model of T2D to investigate whether TFEB activation could help alleviate DE. T2D mice showed cognitive impairment and AD-like pathology, which were alleviated when TFEB was activated by either mTOR inhibition or TFEB overexpression..."

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

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:

"Chronic brain hypoperfusion (CBH) is caused by decreased blood flow to the brain and is considered a key predictor of neurodegenerative diseases such as Alzheimer’s disease and vascular dementia. CBH can indirectly lead to cognitive decline by altering the expression of proteins at synapses, where neurons communicate through neurotransmitters released from presynaptic vesicles and recognized by postsynaptic receptors. Researchers recently linked this decline to the microRNA miRNA-153. FM 1-43 experiments showed that overexpression of miRNA-153 impairs presynaptic vesicle release, and in a CBH rat model, overexpression of miRNA-153 decreased the expression of multiple proteins involved in vesicle release. Conversely, knockdown of miRNA-153 rescued these synaptic defects and attenuated cognitive decline in the rat model..."

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

We asked people diagnosed with Alzheimer's to tell us memories they never want to forget.

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:

"Micro-RNAs are small, non-coding molecules no bigger than a couple dozen nucleotides in length. But don’t let their size fool you. While they may not code for proteins, themselves, these molecules play an important role in many biological processes by regulating the expression of genes. Recently, they have been implicated in neuron development and neurodegenerative diseases such as Alzheimer’s. Now, a recent study published in the journal, _Molecular Neurodegeneration_, has identified a previously unreported association between the amount of a particular microRNA and the accumulation of toxic proteins that characterizes Alzheimer’s disease. Late-onset Alzheimer’s is characterized by structural changes in the brain and a decline in cognitive abilities, such as memory loss, that worsens with age. Despite the high prevalence of this disease and research efforts, its precise causes are still being worked out. Recent research, though, suggests altered gene expression by non-coding RNAs may play a role..."

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