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LBD: Understand Lewy body spreading and interactions with other AD/ADRD-related pathologies (Milestone 2.M)

AD Related Dementias Focus

Identify mechanisms by which Lewy body diseases may spread between and affect different brain regions and how Lewy bodies interact with other pathologies.


Success Criteria

  • Support research investigating α-synuclein spreading and α-synuclein interactions with β-amyloid, tau, TDP-43 and other proteins and pathologies associated with dementia.

Summary of Key Accomplishments

NINDS currently supports a Center Without Walls with four separate projects that are devoted to understanding devoted to understanding how the protein alpha-synuclein, which is often associated with LBD and Parkinson's disease, interacts with other AD/ADRD-related abnormal proteins, like beta-amyloid and tau, to initiate or accelerate brain disease in LBD. A request for applications (RFA NS21-006) was issued to invite research that seeks to understand how alpha-synuclein spreads and causes damage in the nervous system, and a number of applications were received and funded. Two recent research studies have shown that injecting alpha-synuclein into the brains of mice that carry gene mutations associated with Alzheimer's disease accelerates the rate at which beta-amyloid clumps deposit in the brain. These studies also show that abnormal deposits of tau and alpha-synuclein increase and brain inflammation increases.

This information is current as of July 2022.


Research Implementation Area
Research on Disease Mechanisms
Timeline
2016–2025
Status
In Progress

Accomplishments/Implementation Activities

Funding Initiatives

Research Programs and Resources

Relevant Recommendations

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