Lifeboat Foundation

In a new #Stanford study explaining the cellular mechanisms behind cognitive impairment from chemotherapy, scientists have demonstrated that a widely used chemotherapy drug, #methotrexate, causes a complex set of problems in three major cell types within the brain’s white matter. The study also identifies a potential remedy.

In a new study explaining the cellular mechanisms behind cognitive impairment from chemotherapy, scientists have demonstrated that a widely used chemotherapy drug, methotrexate, causes a complex set of problems in three major cell types within the brain’s white matter. The study also identifies a potential remedy.

Eyewitness testimony is unreliable because people try to understand a traumatic event by using what they know about the world and fill in gaps, experts said.

By the time he was diagnosed with metastatic melanoma, Luke Simons, now 83, had already watched his wife and his longtime business partner struggle with cancer. His wife had chemo for her breast cancer 20 years ago. His business partner with multiple myeloma died 5 years ago. “I was obviously aware of what it could do,” he says of cancer. And of chemo, “my God, that can be just horrible what that can do to you.”

As soon as he got the diagnosis, Simons’ doctor at Vanderbilt-Ingram Cancer Center (where his wife is on the board) told him about how president Jimmy Carter’s metastatic melanoma had just become undetectable after taking Merck’s new drug Keytruda, which enables a person’s immune system to recognize and attack cancer cells. The doctor gave Simons the option of Keytruda, and he took it.

After his first dose, Simons developed pneumonitis, which he aptly describes as a “fever in my lungs,” that made his doctor question whether to continue the treatment. He did, and the cancer that had spread to Simons’ brain and pancreas is not showing up on scans, three years later.

Continue reading “Can Cancer Care Be Industrialized? Vanderbilt And GE Are Teaming Up To Find Out” »

A new study has discovered that patients with high blood pressure and abnormalities in the periventricular white matter in the brain showed signs of cognitive impairment despite taking medication to lower their blood pressure.

High blood pressure has been linked to an increased risk for dementia, but what’s unclear is what kinds of subtle negative changes take place in the brain that may affect cognitive function, according to researchers. Finding new ways to detect minor types of cognitive impairment may help determine who is at risk for early-stage dementia, they noted.

In the study, researchers looked at 345 men and women with a median age of 65 who had high blood pressure.

Continue reading “High Blood Pressure Implicated in Cognitive Impairment” »

A stroke or a “brain attack” can have life-threatening consequences just like a heart attack. However, there are some early signs of a stroke that start showing up as early as a month before it actually happens. Here are seven such symptoms—knowing them might save someone’s life.

Strokes happen when a blood vessel transporting oxygen to the brain bursts or gets obstructed by a clot. As a result, the brain doesn’t receive much oxygen and the brain cells start to die off. The functions controlled by the affected part of the brain will not be performed normally, and this will have a huge impact on health.

A stroke can manifest differently in every individual, but one thing in common is that it initiates suddenly. Read below the most common symptoms that manifest one month before a stroke, and if you are experiencing any of these, think about consulting your doctor.

Continue reading “7 Early Warning Signs of ‘Brain Attack’ That Appear Almost 1 Month Before Stroke” »

Plant cognitive ecologist Monica Gagliano talks about the challenges facing serious scientific research into plant intelligence.

Many scientists research the practical and immediate applications of bio molecular technology but it seems most fail to study our most important, and largest organ, our skin.

Who will officially be the first transhuman? Will it be you? Why wait decades? This article explains one approach to speeding up the process and also the challenge involved.

Defining the Object of the Goal:

Continue reading “Becoming the First Transhuman: A Call For The Right Stuff” »

A new neurostimulator developed by engineers at UC Berkeley can listen to and stimulate electric current in the brain at the same time, potentially delivering fine-tuned treatments to patients with diseases like epilepsy and Parkinson’s.

The device, named the WAND, works like a “pacemaker for the brain,” monitoring the brain’s electrical activity and delivering electrical stimulation if it detects something amiss.

These devices can be extremely effective at preventing debilitating tremors or seizures in patients with a variety of neurological conditions. But the electrical signatures that precede a seizure or tremor can be extremely subtle, and the frequency and strength of electrical stimulation required to prevent them is equally touchy. It can take years of small adjustments by doctors before the devices provide optimal treatment.

Continue reading “Wireless ‘pacemaker for the brain’ could be new standard treatment for neurological disorders” »

Brain accumulation of the amyloid-β (Aβ) peptide is believed to be the initial event in the Alzheimer disease (AD) process. Aβ accumulation begins 15–20 years before clinical symptoms occur, mainly owing to defective brain clearance of the peptide. Over the past 20 years, we have seen intensive efforts to decrease the levels of Aβ monomers, oligomers, aggregates and plaques using compounds that decrease production, antagonize aggregation or increase brain clearance of Aβ. Unfortunately, these approaches have failed to show clinical benefit in large clinical trials involving patients with mild to moderate AD. Clinical trials in patients at earlier stages of the disease are ongoing, but the initial results have not been clinically impressive. Efforts are now being directed against Aβ oligomers, the most neurotoxic molecular species, and monoclonal antibodies directed against these oligomers are producing encouraging results. However, Aβ oligomers are in equilibrium with both monomeric and aggregated species; thus, previous drugs that efficiently removed monomeric Aβ or Aβ plaques should have produced clinical benefits. In patients with sporadic AD, Aβ accumulation could be a reactive compensatory response to neuronal damage of unknown cause, and alternative strategies, including interference with modifiable risk factors, might be needed to defeat this devastating disease.