Neutrino-detecting IceCube teams up with other instruments to study distant galaxy’s “blazar”.
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A disclaimer on the new article that I wrote: while I do think the Beta-amyloid plaque plays a key role in the development of Alzheimer’s disease I do not think it’s the only thing. I’ll be writing more on Alzheimer’s disease as I study more.
The abnormal accumulation β-amyloid peptide is the leading candidate for the cause of Alzheimer’s disease is currently ranked the 6 th leading cause of death in the United States while some statistics claim it may rank as high as the third leading cause of death.
What is Alzheimer’s disease?
Alzheimer’s is a slowly progressive disease that causes the loss of memories and cognitive function. It is the most common form of dementia and accounts for 60 to 80% of cases.
Donald J. Trump added a new photo
Posted in futurism
Based on NASA’s “schedule risk analysis” from April, the agency estimates that Boeing will reach this milestone sometime between May 1, 2019, and August 30, 2020. For SpaceX, the estimated range is August 1, 2019, and November 30, 2020.
Both of the companies are well behind schedule, forcing the agency to scramble.
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The abnormal accumulation β-amyloid peptide is the leading candidate for the cause of Alzheimer’s disease. Alzheimer’s disease is currently ranked the 6th leading cause of death in the United States while some statistics claim it may rank as high as the third leading cause of death.
What is Alzheimer’s disease?
Alzheimer’s is a slowly progressive disease that causes the loss of memories and cognitive function. It is the most common form of dementia and accounts for 60 to 80% of cases.
Alois Alzheimer is credited as documenting the first published case of “presenile dementia.” Later his colleague Kraepelin would identify it as Alzheimer’s disease.
Present treatments for Alzheimer’s are currently ineffective in reversing the effects of Alzheimer’s disease. For well over a decade research has suggested that the precursor of the β-amyloid is implicated in the BACE1 enzyme. Current BACE1 inhibitory drugs are in development to help patients with Alzheimer’s disease.
Xiangyou Hu, pHd and team generated BACE1 conditional knockout (BACE1fl/fl) mice in order to mimic the inhibition of BACE1 in adults. In order to induce the deletion of BACE1 through genetic modification the team also bred BACE1fl/fl mice with ubiquitin-CreER (a genetic inhibitor) after passing early developmental stages.
Results
The reversal of amyloid deposition was the result of sequential and increased deletion of BACE1 in an adult AD mouse model 5xFAD.
Another significant improvement based upon the reversal of amyloid deposition was in gliosis, which is one of the most prominent features of many diseases of the central nervous system. Gliosis is a process which leads to scarring within the central nervous system. It is well established that neurotic dystrophy is induced by Beta-amyloid plaque.
Thus another result of this reversal saw an improvement in less neurotic dystrophy. Moreover, as determined by experiments of contextual fear conditioning and by long-term potentiation, there was vast improvement in synaptic functions.
The results indicate that the reversal of Beta-amyloid deposition through the inhibition of BACE1 in AD mouse models will provide insight for the proper use of BACE1 inhibitor in human patients.
Journal of Experimental Medicine
February 14, 2018
Full Abstract Study
Minoring in the majors
Posted in biotech/medical, life extension
It’s in a bad taste to say that other global issues are more urgent than ageing, when pretty much all global issues—ageing included—affect the life, and the quality of life, of many people.
Suppose you’re in your mid-seventies, and you find out that your aortic valve doesn’t work very well. Undergoing a replacement operation—nowadays, a relatively simple and safe procedure—is not only going to help you with your unpleasant episodes of fatigue, chest pain, and dizziness, it may well save your life, minimizing your risk of sudden cardiac arrest.
Your doctor suggests that you undergo the procedure and sends you to a surgeon for the operation; however, when you get there, the surgeon starts yelling at you that, rather than using resources to replace your valve and extend your life, we should fund initiatives to save children in poor countries, build health clinics, train midwives, and fight for equal opportunity and for women’s rights. He then goes on rambling that, until these issues are addressed, he doesn’t want to hear about extending your natural lifespan—after all, since you’re in your mid-seventies, you’re well above the world’s average lifespan; he shoos you and your family out and slams the door on you.
The chances are good that you’d think this person was several sandwiches short of a picnic; you would report him and have him fired for malpractice. Thankfully, you’re not very likely to run into a surgeon like that, but you are likely to bump into people contending the exact same things as the mad surgeon when you replace heart surgery—a very specific form of life extension—with the general concept of life extension. Why is that?
Pills hailed as the first real “anti-aging” drugs inched a little closer to the market after a study found they cut the number of respiratory infections in the elderly by half.
The drugs: The pills act on an aging-related pathway called TORC1. Inhibiting this pathway “has extended life span in every species studies to date” (like mice and worms), according to Joan Mannick, who lead the study for drug giant Novartis.
Will humans live longer, too? Maybe. But that will take time to figure out. For now, what’s known is that giving people 65 and older these drugs seems to boost their immune function. Elderly people taking the drugs got about 40 percent fewer colds or bronchial infections. About 264 people got the drugs over six weeks and then were tracked for a year.
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