This patient education program explains amyotrophic lateral sclerosis (ALS or Lou Gehrig's …
This patient education program explains amyotrophic lateral sclerosis (ALS or Lou Gehrig's Disease) including the causes, symptoms, diagnosis and treatment options. This resource is a MedlinePlus Interactive Health Tutorial from the National Library of Medicine, designed and developed by the Patient Education Institute.
This resource is a video abstract of a research paper created by …
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:
"A new clinical trial suggests levosimendan could improve respiratory function in patients with amyotrophic lateral sclerosis. ALS is an adult-onset neurodegenerative disease that results in progressive weakness. Those affected by the disease typically die within three to four years of diagnosis due to respiratory failure commonly resulting from weakening of the diaphragm. Prior studies indicate that levosimendan – a calcium sensitizer on the market since 2000 for the treatment of acute worsening of severe heart failure – can also boost the force and efficiency with which the diaphragm contracts. This prompted researchers to investigate whether levosimendan is clinically beneficial to those with ALS. The phase 2 trial used a randomized, double-blind, placebo-controlled, crossover design to evaluate the efficacy and safety of oral levosimendan in 66 patients with ALS..."
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 …
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:
"People often take probiotics to supplement the community of microbes living in their gut and maintain their digestive health. But can gut microbes also have an important effect on the brain? New evidence indicates that they can, with possible key roles in neurologic disorders such as Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis (ALS). While treatment with antibiotics to manipulate the gut microbiota has been shown to improve neurologic symptoms, it can worsen them in SOD1 mice, which are often used to study ALS. To better understand the role of gut microbes in ALS, scientists either depleted the gut microbiota of SOD1 mice with antibiotics or augmented it by housing SOD1 with non-SOD1 mice to encourage microbial transfer. The antibiotic treatment decreased motor function and survival in the SOD1 mice, while cohabitation with non-SOD1 mice had no effect..."
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 …
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:
"Amyotrophic lateral sclerosis (ALS) is a devastating, fatal neurodegenerative disease. One of the likely mechanisms of ALS degeneration is a calcium (Ca²⁺) imbalance in neurons. The neurotoxin L-BMAA causes ALS-like symptoms, likely by causing a Ca²⁺ ‘leak’ in the endoplasmic reticulum (ER) leading to cell stress and death. The enzyme SOD1 and its non-metallated form ApoSOD1 can prevent cell death from L-BMAA. Both forms of SOD1 do this by rapidly increasing the concentration of Ca²⁺ in the ER, but the intermediary mechanism is not yet understood. However, a recent study suggested that the sodium/calcium ion (Na⁺/Ca²⁺) exchanger protein, NCX1, mediates this increase in Ca²⁺ concentration. Both forms of SOD1 activated NCX1 in its ‘reverse mode’ where it pumps Ca²⁺ back into the ER, counteracting the leak. This was likely achieved by a prior SOD1-induced increase in the Na⁺ concentration..."
The rest of the transcript, along with a link to the research itself, is available on the resource itself.
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