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New clues to serious neurodegenerative diseases

New clues to serious neurodegenerative diseases


Dementia includes various neurodegenerative conditions that cause memory loss and cognitive impairment and affect some people. 55 million people World wide. However, despite dementia’s prevalence, there are few effective treatments. One reason is that scientists still do not understand exactly how dementia occurs at the cellular and molecular level.

Now, a team led by scientists from Harvard Medical School and the Harvard TH Chan School of Public Health is working to unravel the mechanisms underlying a form of dementia that develops early in life.

in a study October 7 Nature Communicationsresearchers have found that a genetic form of frontotemporal dementia (FTD) is associated with the accumulation of specific lipids in the brain–; due to

Results based on experiments in human brain cells and animal models may provide new insights into FTD and aid in the design of new therapeutics. Furthermore, the findings highlight mechanisms of metabolic disruption that may be associated with other forms of neurodegeneration, the researchers say.

Black box

There are several different types of dementia, each with complex genetics with various mutations. Characterized by loss of cells in the frontal and temporal lobes of the brain, FTD is 5 to 10 percent of dementia cases.often diagnosed in patients between 45 and 65, genetic forms tend to cluster in families. About 15% of the time, FTD is associated with a specific mutation in the GRN gene that causes brain cells to stop producing a protein called progranulin.

Previous studies have linked progranulin to parts of the cell called lysosomes, which are responsible for intracellular cleanup and other metabolic activities. However, “protein function remains a black box, including its role in the lysosome,” said co-lead authors. Wade HarperBert and Natalie Vallee Professor of Molecular Pathology, Department of Cell Biology, Bravatnik Institute, HMS.

Harper collaborated on the study with co-lead author Tobias Walther When Robert Farese Jr.At the time of his research, he was Professor of Cell Biology at HMS and Professor of Molecular Metabolism at the Harvard Chan School. Fellow of the Harper Institute.

The researchers initially found that gangliosides accumulated in progranulin-deficient human cell lines and mouse brains, as well as in brain cells from FTD patients. A lipid commonly found throughout the nervous system.

The team then used a recently developed lysosome purification technique to analyze the types and amounts of proteins and lipids present within the lysosomes. Using this technique, scientists found that lysosomes in these cells and tissues from brains with FTD had reduced levels of progranulin and lower than normal levels of a lipid called BMP. Found in the central nervous system. But when the researchers added her BMPs to cells, they observed that these cells accumulated much lower levels of gangliosides.

Taken together, this finding suggests that progranulin in lysosomes helps maintain BMP levels necessary to prevent gangliosides from accumulating in brain cells. Buildup that can contribute to FTD.

“We have identified a role for progranulin in supporting the proper breakdown of gangliosides,” Farese said, while also showing that the problem could be corrected.

“People are already working on treatments that involve giving patients a source of progranulin, and our results are consistent with that approach being potentially therapeutically beneficial,” said Walther. He added that it may also be possible to develop therapies that focus on replacement of BMPs rather than progranulin and target different parts of the mechanism, he said.

Researchers also believe that similar lysosome-based mechanisms may be relevant to neurodegenerative diseases beyond FTD. The ideas they point out are quickly taking hold in the field.

“Lysosomes may be a key feature of many types of neurodegenerative diseases, all of which may be associated with lysosomes in different ways,” Harper said. increase. For example, scientists already know that proteins involved in genetic forms of Parkinson’s disease control aspects of lysosomal function. Farese added that further research is needed to understand exactly how different lipids and proteins interact with lysosomes in the context of various neurodegenerative diseases.

Researchers are now studying several genes related to lysosomal function, including those associated with lysosomal storage diseases, to find connections between them. The remaining central question is how progranulin raises her BMP levels in the brain. Additional research is needed to further elucidate the mechanistic steps the team uncovered and explain how lipid accumulation leads to cognitive decline.

“This study shows the power of working together and following science,” says Walther. “Using the right tools and asking the right, detailed questions can sometimes lead to unexpected discoveries.”

Funding and authorship

Additional authors include Johannes Amber, Pedro Maria, Ruth Richards, Alexander Fischer, Shubham Singh, and Joan Paulo from HMS and the Harvard Chan School. Her Geetika Aggarwal and Andrew Nguyen from St. Louis University Medical School. Salvatore Spina, Alissa Nana, Lea Grinberg, and William Seeley from the University of California, San Francisco. Michal Surma and Christian Klose of Lipotype GmbH.

This study was supported by the Bluefield Project to Cure FTD, the National Institutes of Health (R01NS083524; R01GM132129), Google Ventures, Third Rock Ventures, Aligning Science Across Parkinson’s (ASAP-000282) initiative, Canadian Institutes of Health Research, and Howard Hughes. medical laboratory.




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