Involvement of inflammation in Alzheimer’s disease pathogenesis and therapeutic potential of anti-inflammatory agents

Aug 21, 2015Archives of pharmacal research

Role of inflammation in Alzheimer's disease and possible benefits of anti-inflammatory treatments

AI simplified

Circadian Biology on OpenScience ↗PubMed ↗DOI ↗

Abstract

Alzheimer's disease may be significantly influenced by neuroinflammation.

Beta-amyloid peptide fibrils and neuroinflammation are key characteristics of Alzheimer's disease.
Risk factors linked to Alzheimer's include the accumulation of beta-amyloid, hyperphosphorylation of tau protein, and neuroinflammation.
Epidemiologic studies suggest that anti-inflammatory drugs could reduce the incidence of Alzheimer's disease.
Astrocytes, microglia, and peripheral immune cells may contribute to neuroinflammation and neurodegeneration in the brains of Alzheimer’s patients.
Recent data indicate that microRNAs may influence the brain's neuroinflammatory responses.

AI simplified

Alzheimer's disease (AD) is the most common form of dementia. It is characterized by beta-amyloid (Aβ) peptide fibrils, which are extracellular depositions of a specific protein, and is accompanied by extensive neuroinflammation. Various studies have demonstrated risk factors that can affect AD pathogenesis, and they include accumulation of Aβ, hyperphosphorylation of tau protein, and neuroinflammation. Among these detrimental factors, neuroinflammation has been highlighted by epidemiologic studies suggesting that use of anti-inflammatory drugs could significantly reduce the incidence of AD. Evidence suggests that astrocytes, microglia, and infiltrating immune cells from periphery might contribute to or modify the process of neuroinflammation and neurodegeneration in AD brains. In addition, recent data indicate that microRNAs may affect neuroinflammatory responses in the brain. This article focuses on supportive evidence that neuroinflammation plays a critical role in AD development. In addition, we depict putative therapeutic capacity of anti-inflammatory drugs for AD prevention or treatment. We also discuss pathogenic mechanisms by which astrocytes, microglia, T cells and microRNA participate in AD and the neuroprotective mechanisms of anti-inflammatory drugs.

Full Text

Full text is available at the source.

View full text (PDF) ↗View full text (HTML) ↗View full text ↗

Involvement of inflammation in Alzheimer’s disease pathogenesis and therapeutic potential of anti-inflammatory agents

Abstract

Full Text

You found one interesting study. We’ll send the next 7.

what lands in your inbox each week:

Recent issues from the circadian biology brief

Abstract

Full Text

Related papers

You found one interesting study. We’ll send the next 7.

what lands in your inbox each week:

Recent issues from the circadian biology brief