The shingles vaccine has been found to lower the risk of heart disease for up to eight years, according to a recent study published in the European Heart Journal. The study, which included over 1.2 million people aged 50 or older living in South Korea, revealed that those who received the vaccine had a 23% lower risk of cardiovascular events, including stroke, heart failure, and coronary heart disease.

The protective effect of the vaccine was particularly pronounced for men, younger individuals (under 60), and those with unhealthy lifestyles such as smoking, drinking alcohol, and being inactive. The study’s findings suggest that vaccination could offer health benefits beyond preventing shingles, a painful rash caused by the varicella zoster virus.

Led by Professor Dong Keon Yon from the Kyung Hee University College of Medicine in Seoul, South Korea, the research team aimed to investigate whether getting vaccinated against shingles could lower the risk of heart problems associated with the condition. Their study involved gathering data on cardiovascular health and other factors that can influence health, such as age, sex, wealth, and lifestyle, for individuals who received the live zoster vaccine between 2012 and 2020.

The researchers found that among people who received the vaccine, there was a 23% lower risk of cardiovascular events overall, with a 26% lower risk of major cardiovascular events (a stroke, heart attack or death from heart disease), a 26% lower risk of heart failure, and a 22% lower risk of coronary heart disease. The protective effect was strongest in the two to three years after the shingles vaccine was given, but researchers found that the protection lasted for up to eight years.

The study’s findings have significant implications for public health policy and could lead to changes in vaccination recommendations to include cardiovascular benefits. However, as Professor Yon noted, more research is needed on the recombinant vaccine, which is now being used in many countries, to confirm its effectiveness in reducing heart disease risk.

The latest study published in Cell has revealed that phosphoglycerate dehydrogenase (PHGDH), previously known as a biomarker for early detection of Alzheimer’s disease, is actually a causal gene for spontaneous Alzheimer’s. Using artificial intelligence to visualize the three-dimensional structure of PHGDH, researchers at the University of California San Diego discovered a previously unknown regulatory role played by the protein.

The study found that altering PHGDH expression levels had consequential effects on Alzheimer’s disease progression in mice and human brain organoids. Lower levels corresponded to less disease progression, whereas increasing the levels led to more disease advancement. This established that PHGDH is indeed a causal gene for spontaneous Alzheimer’s disease.

In further support of this finding, the researchers determined that PHGDH triggers a pathway that disrupts how cells in the brain turn genes on and off, leading to issues such as the development of Alzheimer’s disease.

The research team used AI again to identify NCT-503, a small molecule with the potential to inhibit PHGDH’s regulatory role. They tested NCT-503 in two mouse models of Alzheimer’s disease and observed that it significantly alleviated Alzheimer’s progression, demonstrating substantial improvement in memory and anxiety tests.

While there are limitations to their study, the results are promising, according to lead author Sheng Zhong. “Now there is a therapeutic candidate with demonstrated efficacy that has the potential of being further developed into clinical tests,” he said.

“The next steps will be to optimize the compound and subject it to FDA IND-enabling studies.” An advantage of small molecules is that they could even be administered orally, unlike current treatments that require infusions.

Parkinson’s disease is a neurodegenerative disorder that affects millions worldwide. Traditionally, it was diagnosed in its late stage based on motor symptoms, by which time the brain had already suffered significant damage. However, researchers from the PRODI Center for Protein Diagnostics at Ruhr University Bochum, Germany, and betaSENSE have made a groundbreaking discovery – a reliable biomarker in the spinal fluid that enables early diagnosis of Parkinson’s disease.

The misfolding of alpha-synuclein (αSyn) protein plays a crucial role in the development of Parkinson’s. When αSyn transforms from its normal α-helical structure to a β-sheet-rich structure, it becomes “sticky” and forms larger complexes called oligomers. These oligomers eventually produce long fibrillar filaments that aggregate into macroscopically large Lewy bodies in the brain.

A team led by Professor Klaus Gerwert has successfully detected this misfolding of αSyn in body fluids with a sensitivity and specificity of over 90 percent, using cerebrospinal fluid samples from patients at two Parkinson’s centers. The measurements were carried out using betaSENSE’s patented iRS (immuno-infrared sensor) technology.

This breakthrough is not only significant for diagnosing Parkinson’s but also has the potential to revolutionize the development of new treatments. By identifying early-stage disease, researchers can explore more effective therapeutic options and potentially slow down or halt the progression of the disease.

The successful implementation of iRS technology in Alzheimer’s diagnosis has shown that it can accurately predict the risk of dementia up to 17 years before clinical diagnosis. Similarly, this approach for αSyn misfolding in Parkinson’s can shed light on the progression of the disease and the efficacy of treatments.

This discovery brings hope to millions worldwide, offering a new window into early diagnosis and treatment of this debilitating condition.