Oligodendrocytes and Alzheimer's disease

  title={Oligodendrocytes and Alzheimer's disease},
  author={Zhiyou Cai and Ming Xiao},
  journal={International Journal of Neuroscience},
  pages={104 - 97}
  • Z. Cai, M. Xiao
  • Published 1 February 2016
  • Biology
  • International Journal of Neuroscience
Extensive evidence has indicated that the breakdown of myelin is associated with Alzheimer's disease (AD) since the vulnerability of oligodendrocytes under Alzheimer's pathology easily induces the myelin breakdown and the loss of the myelin sheath which might be the initiating step in the changes of the earliest stage of AD prior to appearance of amyloid and tau pathology. Considerable research implicated that beta-amyloid (Aβ)-mediated oligodendrocyte dysfunction and myelin breakdown may be… 
Oligodendroglial Cells in Alzheimer's Disease.
Therapies that target NG2-glia are likely to have positive effects on myelination and neuroprotection in AD, and the hypothesis that a vicious cycle of myelin loss and failure of regeneration from NG2 -glia plays a key role in AD is proposed.
Role of Neuron and Glia in Alzheimer’s Disease and Associated Vascular Dysfunction
Overall, the current review informs about the interaction of neuronal and glial cell types in AD pathogenesis and its critical association with cerebrovascular dysfunction.
Iron Pathophysiology in Alzheimer's Diseases.
Future research will focus on iron as an opportunity to study the mechanism of the occurrence and development of AD from the iron steady state to more fully clarify the etiology and prevention strategies.
Unravelling the glial response in the pathogenesis of Alzheimer's disease
A review of recent studies attempting to unravel the glial response during the course of disease and how this action may dictate the outcome of neurodegeneration examines the importance of regional heterogeneity of glial cells within the CNS during healthy aging and disease.
Molecular Bases of Alzheimer’s Disease and Neurodegeneration: The Role of Neuroglia
The main physiological functions of the glial cells are described and the link between neuroglia and the most studied molecular bases of AD is discussed, with particular attention to their role in terms of neurodegeneration.
The neuroinflammatory interleukin-12 signaling pathway drives Alzheimer’s disease-like pathology by perturbing oligodendrocyte survival and neuronal homeostasis
IL-12, but not IL-23 is the main driver of AD-specific IL-12/IL-23 neuroinflammation, which alters neuronal and oligodendrocyte functions, and may foster first clinical trials in AD subjects using this novel neuroimmune target.
Blood-Based Biomarkers of Neuroinflammation in Alzheimer’s Disease: A Central Role for Periphery?
Interestingly, as a result of the bidirectional communication between the brain and the periphery, the blood compartment ends up reflecting several pathological changes occurring in the AD brain and can represent an accessible source for such biomarkers.


Early oligodendrocyte/myelin pathology in Alzheimer's disease mice constitutes a novel therapeutic target.
It is demonstrated that Abeta(1-42) leads to increased caspase-3 expression and apoptotic cell death of both nondifferentiated and differentiated mouse oligodendrocyte precursor (mOP) cells in vitro and may help to validate new therapeutic options designed to avert these early impairments in Alzheimer's disease.
Alzheimer's disease as homeostatic responses to age-related myelin breakdown
Inflammatory process in Alzheimer's Disease
Clinical trials and animal models with non-steroidal anti-inflammatory drugs (NSAIDs) indicate that these drugs may decrease the risk of developing AD and apparently reduce Aβ deposition.
Age-related myelin breakdown: a developmental model of cognitive decline and Alzheimer’s disease
Human brain myelination and amyloid beta deposition in Alzheimer’s disease
Quantifying age-related myelin breakdown with MRI: novel therapeutic targets for preventing cognitive decline and Alzheimer's disease.
This myelin-centered model together with the technology that makes it possible to measure the trajectory of myelin breakdown provide a framework for developing novel treatments, as well as assessing efficacy of currently available treatments, intended to slow or reverse the breakdown process in both clinically healthy aswell as symptomatic populations.
Microglia, neuroinflammation, and beta-amyloid protein in Alzheimer's disease
Compelling evidence from basic molecular biology has demonstrated the dual roles of microglia in the pathogenesis of Alzheimer's disease (AD). On one hand, microglia are involved in AD pathogenesis
Amyloid-β Peptides Are Cytotoxic to Oligodendrocytes
It is demonstrated that Abeta 1-40 and a truncated fragment, Abeta 25-35, induced death of oligodendrocytes (OLGs) in vitro in a dose-dependent manner with similar potencies and suggest that oxidative injury contributes to Abeta cytotoxicity in OLGs.
Dynamic changes in myelin aberrations and oligodendrocyte generation in chronic amyloidosis in mice and men
It is demonstrated that oligodendrocyte progenitors specifically react to amyloid plaque deposition in an AD‐related mouse model as well as in human AD pathology, although with distinct outcomes.
Glial Cells in Alzheimer’s Disease
Two salient neuropathological features: intraneuronal neurofibrillary tangles and complex neuritic β-amyloid-containing plaques are accompanied by progressive neuronal loss and decreased density of synaptic elements within the cerebral cortical neuropil.