Reactive gliosis in Alzheimer's disease: a crucial role for cognitive impairment and memory loss.
Ricardo Augusto Leoni De SousaPublished in: Metabolic brain disease (2022)
Alzheimer's disease (AD) is a neurodegenerative disorder that leads to cognitive decline and memory loss. Insulin resistance in central nervous system (CNS) is a common feature in dementia. Defective insulin signaling is associated to higher levels of inflammation and to neuronal dysfunction. A reactive gliosis, a change that occurs in glial cells due to damage in CNS, seems to be one of the most important pro-inflammatory mechanisms in AD pathology. The first response to CNS injury is the migration of macrophages and microglia to the specific site of the injury. Oligodendrocytes are also recruited to to contribute with remyelination. The last component of a reactive gliosis is astrogliosis, which is the enhancement of astrocytes expression with concomitant changes in its morphology being the main cells of the glial scar. Here, we review the mechanisms by which a reactive gliosis can induce or contribute to the development and progression of AD.
Keyphrases
- cognitive decline
- mild cognitive impairment
- induced apoptosis
- cognitive impairment
- oxidative stress
- cell cycle arrest
- blood brain barrier
- neuropathic pain
- poor prognosis
- working memory
- endoplasmic reticulum stress
- cell death
- machine learning
- inflammatory response
- signaling pathway
- weight loss
- insulin resistance
- cerebrospinal fluid
- cell proliferation
- pi k akt