Friday December 13, 2019
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A new blood test developed to predict TB

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Image source- sites.bu.edu

Seattle: An international team of researchers has identified biological markers in the blood that can help doctors predict who is at high risk of developing active tuberculosis (TB).

One-third of the world’s population is thought to be infected with Mycobacterium tuberculosis (Mtb), the bacterium that causes tuberculosis, but just a small fraction ever develops symptomatic illness.

If validated through additional clinical trials, a test based on these blood biomarkers that the researchers have now identified would allow doctors to target therapies to at-risk people, thus preventing them from getting sick.

The decade-long research effort was led by investigators from the South African Tuberculosis Vaccine Initiative at the University of Cape Town, and the Center for Infectious Disease Research, Seattle, US.

The findings were published in the journal The Lancet.

The biomarkers were identified in two stages. First, researchers collected blood samples for two years from more than 6,000 Mtb-infected but otherwise healthy adolescent volunteers in South Africa.

Analysis of the samples revealed patterns of gene expression that differed between volunteers who eventually developed TB and those who remained healthy.

This risk “signature,” confined to a set of 16 genes, could be detected in a blood sample as early as 18 months before the infected person developed active TB.

Next, the team confirmed the genetic risk signature’s predictive ability in a study of more than 4,500 volunteers in South Africa and The Gambia.

The second study group was more varied in age, health status, ethnicity and exposure to locally common strains of Mtb than volunteers in the first study.

Despite the differences, the same risk signature found in the first study was detected in the people who eventually developed active TB during the second trial. (IANS)

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Having Keto Diet Can Help You Fight Against Alzheimer’s Disease: Research

"Increasing SIRT3 levels via ketone consumption may be a way to protect interneurons and delay the progression of Alzheimer's disease," report researchers

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In Alzheimer's disease, patients start losing memory. Pixabay

Eating low-carb and high-fat diet can help you fight against Alzheimer’s disease, by protect neurons from death during the progression of Alzheimer’s disease, according to new research in mice.

“Ketogenic” is a term for a low-carb diet (like the Atkins diet). The idea is for you to get more calories from protein and fat and less from carbohydrates. You cut back most on the carbs that are easy to digest, like sugar, soda, pastries and white bread.

Early in the development of Alzheimer’s disease, the brain becomes over excited, potentially through the loss of inhibitory, or GABAergic, interneurons that keep other neurons from signaling too much.

Because interneurons require more energy compared to other neurons, they may be more susceptible to dying when they encounter the Alzheimer’s disease protein amyloid beta.

Amyloid beta has been shown to damage mitochondria – the metabolic engine for cells – by interfering with SIRT3, a protein that preserves mitochondrial functions and protects neurons.

health, dementia, walking, Alzheimer
The suffering that comes as a consequence of this disease is enormous. Pixabay

Researchers from the Society for Neuroscience genetically reduced levels of SIRT3 in mouse models of Alzheimer’s disease.

Mice with low levels of SIRT3 experienced a much higher mortality rate, more violent seizures and increased interneuron death compared to the mice from the standard Alzheimer’s disease model and control mice.

However, the mice with reduced levels of SIRT3 experienced fewer seizures and were less likely to die when they ate a diet rich in ketones, a specific type of fatty acid.

Also Read: Almost 60% Indian Organisations to Have their Complete Data on Cloud by Year 2030, Says IBM Survey

The diet also increased levels of SIRT3 in the mice.

“Increasing SIRT3 levels via ketone consumption may be a way to protect interneurons and delay the progression of Alzheimer’s disease,” report researchers. (IANS)