Thursday January 23, 2020

Treating Diabetes May Also Prevent People From Developing Alzheimer’s Disease: Study

In addition, nearly 530 participants had normal blood sugar levels while 250 had prediabetes

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

Treating Type-2 diabetes may prevent people from developing Alzheimer’s disease, says a new study.

Patients with untreated diabetes develop signs of Alzheimer’s disease 1.6 times faster than people who did not have diabetes, according to the study published in the journal Diabetes Care.

Scientists consider Alzheimer’s as the result of a cascade of multiple problems including factors ranging from pollution exposure and genetics to heart and metabolic diseases.

“It is possible that the medicines for treating diabetes might make a difference in the progression of brain degeneration,” said Daniel A. Nation, Associate Professor at University of Southern California.

“But it’s unclear how exactly those medications might slow or prevent the onset of Alzheimer’s disease, so that is something we need to investigate,” he added.

Cognitive Impairment
Alzheimer’s disease patient Isidora Tomaz, 82, sits in an armchair in her house in Lisbon, Portugal. It’s predicted that by 2050, 135 million Americans are going to suffer from mild cognitive impairment, a precursor of Alzheimer’s. VOA

For the study, the researchers analysed data on nearly 1,300 people aged 55 and older.

Data included biomarkers for diabetes and vascular disease, brain scans and a range of health indicators, including performance on memory tests.

Among 900 of those patients, more than 50 had Type-2 diabetes who did not receive any treatment, whereas nearly 70 were undergoing treatment.

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In addition, nearly 530 participants had normal blood sugar levels while 250 had prediabetes.

“Our findings emphasise the importance of catching diabetes or other metabolic diseases in adults as early as possible,” Nation said.

“Among people with diabetes, the difference in their rate of developing the signs of dementia and Alzheimer’s is clearly tied somehow to whether or not they are on medication for it,” he noted. (IANS)

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Drugs That Treat Arthritis in Dogs Can Kill Cancer Cells: Study

Drug for arthritis in dogs can fight cancer in people

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Cancer Cells
Drugs for diabetes, inflammation, alcoholism and even for treating arthritis in dogs can also kill cancer cells. Pixabay

Drugs for diabetes, inflammation, alcoholism — and even for treating arthritis in dogs — can also kill cancer cells in the lab, according to a new health news and study.

The researchers systematically analysed thousands of already developed drug compounds and found nearly 50 that have previously unrecognised anti-cancer activity.

The findings, which also revealed novel drug mechanisms and targets, suggest a possible way to accelerate the development of new cancer drugs or repurpose existing drugs to treat cancer.

“We thought we’d be lucky if we found even a single compound with anti-cancer properties, but we were surprised to find so many,” said study researcher Todd Golub from Harvard University in the US.

Cancer Cells
Most of the non-oncology drugs that killed cancer cells in the study did so by interacting with a previously unrecognized molecular target. (Representational Image). Pixabay

The study, published in the journal Nature Cancer, yet to employ the Broad’s Drug Repurposing Hub, a collection that currently comprises more than 6,000 existing drugs and compounds that are either FDA-approved or have been proven safe in clinical trials (at the time of the study, the Hub contained 4,518 drugs).

Historically, scientists have stumbled upon new uses for a few existing medicines, such as the discovery of aspirin’s cardiovascular benefits.

“We created the repurposing hub to enable researchers to make these kinds of serendipitous discoveries in a more deliberate way,” said study first author Steven Corsello, from Dana-Farber Cancer Institute and founder of the Drug Repurposing Hub.

The researchers tested all the compounds in the Drug Repurposing Hub on 578 human cancer cell lines from the Broad’s Cancer Cell Line Encyclopedia (CCLE).

Using a molecular barcoding method known as PRISM, which was developed in the Golub lab, the researchers tagged each cell line with a DNA barcode, allowing them to pool several cell lines together in each dish and more quickly conduct a larger experiment.

The team then exposed each pool of barcoded cells to a single compound from the repurposing library, and measured the survival rate of the cancer cells.

They found nearly 50 non-cancer drugs — including those initially developed to lower cholesterol or reduce inflammation — that killed some cancer cells while leaving others alone.

Some of the compounds killed cancer cells in unexpected ways.

“Most existing cancer drugs work by blocking proteins, but we’re finding that compounds can act through other mechanisms,” said Corsello.

Cancer Cells
The researchers tested all the compounds in the Drug Repurposing Hub on 578 human cancer cells lines from the Broad’s Cancer Cell Line Encyclopedia. (Representational Image). Pixabay

Some of the four-dozen drugs researchers identified appear to act not by inhibiting a protein but by activating a protein or stabilising a protein-protein interaction.

For example, the team found that nearly a dozen non-oncology drugs killed cancer cells that express a protein called PDE3A by stabilising the interaction between PDE3A and another protein called SLFN12 — a previously unknown mechanism for some of these drugs.

These unexpected drug mechanisms were easier to find using the study’s cell-based approach, which measures cell survival, than through traditional non-cell-based high-throughput screening methods, Corsello said.

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Most of the non-oncology drugs that killed cancer cells in the study did so by interacting with a previously unrecognized molecular target.

For example, the anti-inflammatory drug tepoxalin, originally developed for use in people but approved for treating osteoarthritis in dogs, killed cancer cells by hitting an unknown target in cells that overexpress the protein MDR1, which commonly drives resistance to chemotherapy drugs. (IANS)