Interdisciplinary 础濒锄丑别颈尘别谤鈥檚 disease program
础濒锄丑别颈尘别谤鈥檚 disease (AD) is a progressive brain disorder and the most common form of dementia, affecting ~10% of people over 65 and ~50% of people over 85 years of age. Common features of this devastating disease include clusters of protein aggregates throughout the brain, known as plaques, inflammation of the brain, and changes in brain metabolism, together leading to a drastic decline in cognitive abilities including memory and thinking skills.
Despite AD representing a major health and socioeconomic burden, pharmacological treatments developed to date have been largely ineffective, underscoring a critical and urgent need for innovative strategies for addressing the disease from new perspectives.
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The majority of therapies developed to date have targeted the production of amyloid beta (Ab), the major component of plaques. However, emerging evidence suggests that Ab accumulation is a reactive response to neuronal damage of unknown origin, and not itself the cause of AD.
As these strategies that seek to ameliorate or reverse late-stage disease progression by controlling plaque deposition have so far been unsuccessful, a better approach may be to treat the deficits in brain cells from which AD arises, rather than its symptoms.
Building on recently obtained preliminary data and the unique expertise of each of the affiliated faculty, we are planning an innovative program, consisting of three integrated themes, to tackle AD from new perspectives.
In Theme 1, Drs. Tonks, Lukey, Cheadle, Furukawa, Moses and Van Aelst focus on identifying new molecular targets for AD and develop new drug candidates using cutting-edge click-chemistry techniques.
In Theme 2, Drs. Cheadle, Lukey, Tonks, Moses and Van Aelst harness the unique biology of microglia and target the aberrant inflammatory responses that are a feature of AD, with the goal of validating new therapeutic targets and biomarkers.
In Theme 3, Drs. Tollkuhn, Lukey, Cheadle and Van Aelst address the fact that AD has a more profound impact on women than men, and investigate these differences in the context of understanding protective effects of estrogen-regulated changes in gene expression, and identifying metabolic changes that contribute to the etiology of the disease.
Lucas Cheadle
Hiro Furukawa
Michael Lukey
John Moses
Jessica Tollkuhn
Nicholas Tonks
Linda Van Aelst
We would like to thank our generous donors who support cutting-edge 础濒锄丑别颈尘别谤鈥檚 research at 麻豆传媒社区:
- Christine and Douglas Fox
- Coins for 础濒锄丑别颈尘别谤鈥檚 Research Trust
- Estate of Andre Lacy
- Heartfelt Wings Foundation
- Knott Family Foundation
- The Meier and Linnartz Family Foundation
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