The discovery made by an international research collaboration led by Rutgers University-New Brunswick scientists has shed light on the mysteries surrounding biomolecular condensates – microscopic blobs of protein found in human cells. These enigmatic droplets have been observed to morph from a liquid-like substance, similar to honey, into a hard candy-like solid.

Researchers found that these condensates solidify when they contain a high proportion of alpha-synuclein protein, which is commonly associated with the brain cells of individuals suffering from Parkinson’s disease – a neurodegenerative disorder affecting motor control. The study, published in Science Advances, marks a significant breakthrough in understanding the mechanical properties of biomolecular condensates and their link to various biological functions and diseases.

“We can now better comprehend how diseases like Parkinson’s develop and progress by measuring how these condensates change from liquid to solid in living systems,” said Zheng Shi, an assistant professor at the Department of Chemistry and Chemical Biology in the Rutgers School of Arts and Sciences, and senior author of the study. “This knowledge may lead to novel treatments for neurodegenerative diseases.”

The research team employed advanced technologies to achieve a detailed look at biomolecular condensates – structures lacking a membrane boundary. They have designated them as crucial for understanding cell biology and the origins of disease.

Rutgers scientists have successfully developed tools that allow direct, quantitative measurement of material properties in live cells, overcoming previous limitations that only allowed measurements in test tubes. The technique, which takes advantage of the capillary effect, has enabled researchers to pierce condensates with microscopic pipettes (micropipettes) and measure important properties such as viscosity and surface tension.

“This is an exciting technological leap that opens new avenues for research into the early stages of neurodegenerative diseases and their treatment,” Shi said. “Our goal is to continue measuring and better understand the properties of condensates in living cells, which may have significant implications for disease prevention and treatment.”

Other researchers from Rutgers involved in the study included Jean Baum, Mengying Deng, Jordan Elliott, Zhiping Pang, Xiao Su, and Conor McClenaghan.

The discovery made by this research collaboration has sparked new avenues for understanding neurodegenerative diseases and their potential treatments. The findings may ultimately contribute to the development of novel therapeutic strategies that target biomolecular condensates in live cells, offering hope for individuals affected by these debilitating conditions.

The study published in the American Journal of Human Genetics reveals a groundbreaking approach to understanding Alzheimer’s disease. By integrating computational and functional methods, researchers at Baylor College of Medicine and the Jan and Dan Duncan Neurological Research Institute (Duncan NRI) have identified potential risk factors and targets for therapeutic intervention. The breakthrough findings shed light on the complex causes of Alzheimer’s disease, which affects over 50 million people worldwide.

The study’s lead author, Dr. Juan Botas, emphasized that despite extensive genome-wide studies, the roles of many genes in Alzheimer’s disease were still unclear. “We addressed this issue by integrating published genome-wide association data with multiple computational approaches to identify genes likely involved in AD,” said Dr. Botas. This innovative approach enabled the researchers to pinpoint not only specific genes associated with increased risk but also those that could potentially modulate neuronal dysfunction.

The team systematically assessed 123 candidate genes for their potential impact on Alzheimer’s disease and found that reversing the alterations in 11 of these genes protected fruit flies from damage to their nervous system. Notably, one gene, MTCH2, emerged as a top contender for therapeutic purposes. The researchers discovered that reducing MTCH2 expression in fruit flies aggravated motor dysfunction, while restoring its expression reversed motor impairment and reduced tau accumulation.

“This finding supports further exploration of MTCH2 for therapeutic purposes and highlights the value of a combined computational and experimental approach to uncover main genetic players in Alzheimer’s disease,” said Dr. Botas.

The study’s authors note that this work was supported by NIH grants, underscoring the importance of continued research in this area. As scientists continue to unravel the complexities of Alzheimer’s disease, their findings hold promise for future therapeutic interventions and improved patient outcomes.

The article “Early Menopause Linked to Cognitive Decline: A Study on Women’s Risk Factors” reveals a significant link between early menopause and cognitive decline in women. Researchers from Tohoku University Graduate School of Medicine and Tokyo Metropolitan Institute of Medical Science conducted a study that analyzed the English Longitudinal Study of Ageing, which included 4,726 women and 4,286 men. The team found that women who entered menopause before the age of 40 had worse cognitive outcomes compared to those who entered menopause after the age of 50.

The researchers were motivated by the disproportionate impact of dementia on women worldwide, as well as the association between early menopause and higher risk of depression in later life. The team controlled for modifiable risk factors for dementia and found that menopause at <40 years was significantly associated with worse cognitive function over a two-year follow-up period. Interestingly, the study also showed that hormone replacement therapy (HRT) did not have an association with cognitive function. This suggests that early menopause may be a direct risk factor for cognitive decline in women. The researchers concluded that understanding this relationship could potentially help design treatments to delay the onset of dementia in at-risk patients. The implications of this study are significant, as it highlights the importance of considering sex-specific factors when assessing the risk of developing dementia. Further research is warranted to elucidate the underlying mechanisms of the relationship between levels of female hormones and cognitive function.