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Updated: Jun 6, 2025

Comprehensive Autopsy Program for Individuals with Multiple Sclerosis
Published on: July 19, 2019
Multiple Sclerosis and biological definitions in neurodegenerative diseases
1Department of Clinical Neurosciences, MS Clinic, University of Calgary, Calgary, Alberta, Canada.
Abstract:
Recently, biological definitions in Alzheimer´s disease (AD) and Parkinson´s disease (PD) have been proposed, where clinical descriptors such as "dementia" or "parkinsonism" lost the spotlight. Similar changes are in the horizon in Multiple Sclerosis (MS). However, in MS there is no single molecule (like amyloid) to call the main driver of MS pathogenesis. In fact, there has not been a historically steady candidate. Decades ago T-cells were thought to be paramount, then brain atrophy, and recently the heterogeneous concept of "smoldering disease". There are no established minimal necessary and sufficient conditions for disease pathogenesis in MS. Ethical issues will be important. Technology for biological/biomarker assessments is not universally available and there is risk of overmedicalization. Groups such as the Movement Disorders Society have expressed reservations about pure biological definitions for PD. In MS, we are just in time to tackle these issues in a critical and constructive way.
Insights
Biological definitions are shifting focus from clinical symptoms to underlying mechanisms in neurodegenerative diseases like Alzheimer's and Parkinson's. This abstract discusses the potential shift towards biological definitions in Multiple Sclerosis, highlighting current challenges and ethical considerations.
Area of Science:
- Neuroimmunology
- Neurology
- Biomarker Discovery
Background:
- Recent advances propose biological definitions for Alzheimer's disease (AD) and Parkinson's disease (PD), moving beyond clinical descriptors like dementia or parkinsonism.
- Multiple Sclerosis (MS) is also poised for a similar shift towards biological definitions.
- Unlike AD and PD, MS lacks a single, unifying molecular driver (e.g., amyloid in AD) for its pathogenesis, with historical candidates including T-cells, brain atrophy, and 'smoldering disease'.
Purpose of the Study:
- To explore the implications and challenges of developing biological definitions for Multiple Sclerosis.
- To address the absence of established minimal criteria for MS pathogenesis.
- To proactively consider ethical issues and technological limitations associated with biological assessments in MS.
Main Methods:
- Conceptual analysis of current trends in neurodegenerative disease definition.
- Review of historical and emerging concepts in Multiple Sclerosis pathogenesis.
- Discussion of ethical considerations and technological accessibility for biomarker assessment.
Main Results:
- There is no single, universally accepted molecular driver for Multiple Sclerosis pathogenesis.
- Minimal necessary and sufficient conditions for MS pathogenesis are not yet established.
- Significant ethical considerations and technological disparities exist regarding biological assessments for MS.
Conclusions:
- A critical and constructive dialogue is needed to navigate the transition towards biological definitions in Multiple Sclerosis.
- Addressing ethical concerns and ensuring equitable access to technology are crucial for defining MS pathogenesis.
- Proactive engagement with these issues is timely to guide future research and clinical practice in MS.
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