Analysis of Why Alzheimer's Dementia Never Spontaneously Reverses, Suggests the Basis for Curative Treatment
1Department of Medicine, University of California, 2069 Filbert Street, San Francisco, CA 94123, USA.
Abstract:
A paradox regarding Alzheimer's dementia (AD) and mild cognitive impairment (MCI) is thats spontaneous cure of AD has never been reported, whereas spontaneous cure for MCI occurs fequently. This article analyzes what accounts for this difference. It holds that it is not merely because, for any condition, a stage is reached beyond which it cannot be reversed, since even widely metastatic cancer would be curable were there effective chemotherapy and rheumatoid arthritis became controllable when immune-suppressant treatment was introduced; thus, so could AD be reversible via effective therapy. The analysis presented leads to an explanation of the paradox that is in four categories: (1) levels of transforming growth factor-β are significantly reduced after the transition from MCI to AD; (2) levels of Wnt/β-catenin are significantly reduced after the transition; (3) there is altered epidermal-mesenchymal transition (EMT) in neurons after the transition; (4) there may be risk factors that are either newly operative or pre-existing but worsened at the time of transition, that are particular to individual patients. It is suggested that addressing and ameliorating all of those four categories might cure AD. Medications to address and ameliorate each of the four categories are described.
Insights
Unlike mild cognitive impairment (MCI), Alzheimer's dementia (AD) is not spontaneously reversible. This study identifies four key biological changes and risk factors that may explain this difference and offers potential therapeutic targets for reversing AD.
Area of Science:
- Neuroscience
- Biochemistry
- Pathology
Background:
- A significant paradox exists between Alzheimer's dementia (AD) and mild cognitive impairment (MCI): MCI can resolve spontaneously, while AD has no reported spontaneous cures.
- This difference is not solely due to an irreversible disease stage, as other conditions like metastatic cancer and rheumatoid arthritis have become treatable with targeted therapies.
- Understanding the molecular and cellular differences between MCI and AD is crucial for developing effective treatments for Alzheimer's dementia.
Purpose of the Study:
- To analyze the underlying reasons for the lack of spontaneous recovery in Alzheimer's dementia (AD) compared to mild cognitive impairment (MCI).
- To identify key biological factors and patient-specific risks that differentiate AD from MCI.
- To propose a therapeutic strategy targeting these identified factors to potentially reverse Alzheimer's dementia.
Main Methods:
- Comparative analysis of molecular changes between MCI and AD stages.
- Investigation of transforming growth factor-β (TGF-β) and Wnt/β-catenin signaling pathways.
- Examination of alterations in neuronal epidermal-mesenchymal transition (EMT) and patient-specific risk factors.
Main Results:
- Significantly reduced levels of transforming growth factor-β (TGF-β) observed after the transition from MCI to AD.
- Significantly reduced levels of Wnt/β-catenin signaling pathway components noted following the MCI to AD transition.
- Evidence of altered epidermal-mesenchymal transition (EMT) in neurons and the potential role of new or exacerbated risk factors in AD progression.
Conclusions:
- The transition from MCI to AD is associated with specific molecular changes, including decreased TGF-β and Wnt/β-catenin signaling, and altered neuronal EMT.
- Patient-specific risk factors may also play a critical role in the progression from MCI to AD.
- Targeting these four categories—TGF-β levels, Wnt/β-catenin signaling, neuronal EMT, and risk factors—may offer a potential therapeutic approach to cure Alzheimer's dementia.
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