Alzheimer’s disease (AD) and Parkinson's disease (PD) are the two most widespread neurological disorders
(NDs) characterized by degeneration of cognitive and motor functions due to malfunction and loss of neurons
in the central nervous system (CNS). Numerous evidences have established the role of neuroinflammation in
the AD and PD pathology. The inflammatory components such as microglia, astrocytes, complement system and
cytokines are linked to neuroinflammation in the CNS. More specifically, cytokines have been found to play a central
role in the neuroinflammation of AD and PD. A number of studies have demonstrated abnormally elevated levels
of inflammatory cytokines such as interleukin-1β (IL-1β) and tumor necrosis factor (TNF) in AD and PD patients.
Activated microglial cells have been shown to be involved in the secretion of pro-inflammatory cytokines such as IL-1, IL-6, TNF-α and transforming growth factor-β, thereby contributing towards the progress of NDs. In addition, studies on AD pathogenesis have
demonstrated that microglia produce beta-amyloid protein (Aβ), which by itself is pro-inflammatory and causes activation of several inflammatory
components. Similarly, chronic inflammation caused by microglial cells is the fundamental process involved in the destruction
of neurons associated with dopamine (DA)-production in the brain of PD patients. Hence, there is a need to explore the key inflammatory
components in AD and PD pathogenesis in order to fully understand the root cause and establish a substantial link between these
two disorders. Such knowledge will help in better management and treatment of AD and PD.
Keywords: Alzheimer's disease, Parkinson's disease, inflammation, cytokines, interleukin-1, interleukin-6, tumor necrosis factor-α,
transforming growth factor-β, microglia.
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