Dementia BREAKTHROUGH? Treatment could slow down effects of disease

The protein, LSD1, acts unsettled in the brain of Alzheimer’s disease patients, scientists from Emory University found.

Future treatments or drugs could focus on stabilising the protein, to slow down the effects of dementia.

A study in mice revealed their genes changes when they took out LSD1. Their cells began to enflame and signalling began to break down.

The cell changes were similar to those seen in Alzheimer’s disease, and some other types of frontotemporal dementia.

Researcher working on the study, David Katz, said: “In these mice, we are skipping the aggregated proteins, which are usually thought of as the triggers of dementia, and going straight to the downstream effects.

“If we were just killing brain cells, we wouldn’t expect the patterns of what we see in the mice to look so much like human patients.

“We also wouldn’t necessarily expect LSD1 to be affected in the human patients.”

In the brain, LSD1 is responsible for maintaining order in the genes that are switched off.

When the scientists removed the protein from mice, they found the mice became cognitively impaired, and even paralysed.

Neutrons were dying in the mice, and they lacked aggregated proteins in their brains – just like those thought to drive Alzheimer’s disease and other types of dementia.

Removing the protein unleashed “stresses” on brain cells, Katz said.

This is the first time LSD1 has been linked to neurodegenerative diseases. The researchers plan to continue probing the protein’s role in the diseases.

A future treatment could focus on enhancing the protein’s power to maintain law and order in the brain, the scientists said.

Meanwhile, thousands of dementia patients were dying unnecessarily by the treatment for psychosis, claimed researchers from the University of Exeter.

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