Background: Alzheimer's disease (AD) is a complex neurodegenerative disorder characterized
by the progressive loss of neurons, which typically leads to severe impairments in cognitive
functions including memory and learning. Key pathological features of this disease include the
deposition of highly insoluble amyloid β peptides and the formation of neurofibrillary tangles
(NFTs) in the brain. Mounting evidence also implicates sustained glial-mediated inflammation as a
major contributor of the neurodegenerative processes and cognitive deficits observed in AD.
Methods: This paper provides an overview of findings from both human and animal studies investigating
the role of microglia and astrocytes in AD, and discusses potential avenues for therapeutic
Results: Glial-mediated inflammation is a ‘double-edged sword', performing both detrimental and
beneficial functions in AD. Despite tremendous effort in elucidating the molecular and cellular
mechanisms underlying AD pathology, to date, there is no treatment that could prevent or cure this
disease. Current treatments are only useful in slowing down the progression of AD and helping
patients manage some of their behavioral and cognitive symptoms.
Conclusion: A better understanding of the role of microglia and astrocytes in the regulation of AD
pathology is needed as this could pave the way for new therapeutic strategies.