Exploring Myelin Dynamics and White Matter Integrity in Dementia: A Path Towards Innovative Therapies

Dementia progression involves complex pathological transformations, notably the degeneration of white matter and the demyelination processes, which significantly affect neuronal network activity. Historically underscored, such demyelination was documented in Alzheimer's Disease (AD) by Alois Alzheimer, yet the focus predominantly shifted towards Aβ and tau pathologies over the past century. Recent studies pivot back to myelin damage as potentially the earliest indicator of neuropathy in AD, suggesting it precipitates synaptic dysfunction and subsequent cognitive decline. Concurrently, Aβ and tau pathologies are now recognized to potentially exacerbate myelin damage. Recent findings suggest that myelin is both regulated by and regulates neuronal activity, indicating that control of myelin through stimulation may aid cognitive function in old age, AD, and other forms of dementia with white matter degeneration. This evolving understanding underlines the need for a focus on myelin dynamics to elucidate similarities and differences in the mechanisms behind dementia pathologies and explore potential therapeutic modalities.

Goal
This Research Topic aims to deepen the comprehension of myelin plasticity's role within dementia's spectrum and elaborate on targeted therapeutic strategies that focus on myelin repair and maintenance. Specifically, the objectives include enhancing the current knowledge around the interaction between myelination processes and dementia progression and deliberating on prospective treatments that directly address white matter plasticity. These could range from pharmacological interventions targeting specific biochemical pathways essential for white matter integrity to novel device therapies aimed at the preservation or enhancement of myelin sheath.

Scope and Information for Authors
To gather further insights into dementia pathophysiology related to white matter and its treatment, we welcome submissions of various types of manuscripts supported by the journal (including Brief Research Reports, Perspectives, Protocols, Mini-Review, Original Research, etc.) addressing, but not limited to, the following themes:
- Relationship between myelin damage and the progression of dementia
- Changes in oligodendrocyte progenitors and cells and their implications in mild cognitive impairment and dementia
- Strategies to enhance neuron-oligodendrocyte progenitor cell interactions to promote remyelination
- Involvement of senescent cells with oligodendrocyte progenitor markers on the progression of dementia
- Innovative drug and device therapies aimed at remyelinating processes in aging and in dementia
- Multimodal treatments targeting myelin repair and cognitive function preservation

Articles accepted after peer review will be published and appear online as soon as approved for publication.

The Topic Editors and the Frontiers office would like to express their gratitude to Dr. Aleksandra Rutkowska for her valuable work in initiating and supporting this Research Topic.

Dr. Aylin Cimenser was employed as Fellow and Senior Director of Data Science at Cognito Therapeutics, Inc from 2020 to 2024. The other Topic Editors declare no competing interests with regard to the Research Topic subject.

Keywords: Alzheimer’s disease, white matter, myelin, remyelination, oligodendrocyte progenitor cells, oligodendrocytes, dementia, demyelination, cognitive decline

Important note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.