Degeneration of white matter and demyelination are present in Alzheimer’s Disease (AD), affect neuronal network activity, and may be critical in understanding the disease’s progression. Although myelin impairment in AD has been reported by Alois Alzheimer more than 100 years ago, Aβ and tau pathologies have been the primary focus of attention in defining the disease as well as in finding therapeutic approaches for the disease. Some studies have suggested that myelin damage may be the first neuropathological abnormality in AD which over time contributes to further damage, synaptic dysfunction, and hence cognitive decline. Other studies have highlighted that Aβ and tau pathologies can also contribute to myelin damage. Furthermore, the recent findings that myelin is both regulated by and regulates neuronal activity suggest that control of myelin through stimulation may aid cognitive function both in old age and in AD.
To characterize the disease progression and search for therapeutic approaches, the link between AD, degeneration of white matter, and myelin damage will need to be better understood.
The main goals of this research topic are 1) To survey and advance our current understanding of white matter plasticity and myelination in relation to AD and 2) To discuss therapeutic approaches in AD that involve explicitly targeting white matter plasticity and myelination. Such approaches could involve new drugs that target specific biomolecular pathways involved in regulating and maintaining healthy white matter function as well as device therapies that may achieve this same goal.
We welcome the submission of any type of manuscript supported by the journal (including Original Research, Review, etc.) pertaining to, but not limited to, the following themes:
a) Relation between myelin damage and Aβ and tau pathology
b) Changes in oligodendrocyte progenitor cells and oligodendrocytes during early and later stages of AD
c) Ways to strengthen the synapses between neurons and oligodendrocyte progenitor cells (OPC) to aid maintain or encourage remyelination
d) Relation between senescent cells that express OPC marker proteins and Aβ plaque environment
e) Drug and/or device based therapeutic approaches to maintain or encourage remyelination in the aging and AD brain
f) Combination therapies that could target remyelination along with reducing Aβ and tau pathology
Dr. Aylin Cimenser is Fellow and Senior Director of Data Science at Cognito Therapeutics, Inc. 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
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.
Degeneration of white matter and demyelination are present in Alzheimer’s Disease (AD), affect neuronal network activity, and may be critical in understanding the disease’s progression. Although myelin impairment in AD has been reported by Alois Alzheimer more than 100 years ago, Aβ and tau pathologies have been the primary focus of attention in defining the disease as well as in finding therapeutic approaches for the disease. Some studies have suggested that myelin damage may be the first neuropathological abnormality in AD which over time contributes to further damage, synaptic dysfunction, and hence cognitive decline. Other studies have highlighted that Aβ and tau pathologies can also contribute to myelin damage. Furthermore, the recent findings that myelin is both regulated by and regulates neuronal activity suggest that control of myelin through stimulation may aid cognitive function both in old age and in AD.
To characterize the disease progression and search for therapeutic approaches, the link between AD, degeneration of white matter, and myelin damage will need to be better understood.
The main goals of this research topic are 1) To survey and advance our current understanding of white matter plasticity and myelination in relation to AD and 2) To discuss therapeutic approaches in AD that involve explicitly targeting white matter plasticity and myelination. Such approaches could involve new drugs that target specific biomolecular pathways involved in regulating and maintaining healthy white matter function as well as device therapies that may achieve this same goal.
We welcome the submission of any type of manuscript supported by the journal (including Original Research, Review, etc.) pertaining to, but not limited to, the following themes:
a) Relation between myelin damage and Aβ and tau pathology
b) Changes in oligodendrocyte progenitor cells and oligodendrocytes during early and later stages of AD
c) Ways to strengthen the synapses between neurons and oligodendrocyte progenitor cells (OPC) to aid maintain or encourage remyelination
d) Relation between senescent cells that express OPC marker proteins and Aβ plaque environment
e) Drug and/or device based therapeutic approaches to maintain or encourage remyelination in the aging and AD brain
f) Combination therapies that could target remyelination along with reducing Aβ and tau pathology
Dr. Aylin Cimenser is Fellow and Senior Director of Data Science at Cognito Therapeutics, Inc. 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
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.