Abstract
α-synuclein (α-syn) pathology and loss of noradrenergic neurons in the locus coeruleus (LC) are among the most ubiquitous features of Parkinson’s disease (PD). While noradrenergic dysfunction is associated with non-motor symptoms of PD, preclinical research suggests that the loss of LC norepinephrine (NE), and subsequently its immune modulatory and neuroprotective actions, may exacerbate or even accelerate disease progression. In this review, we discuss the mechanisms by which α-syn pathology and loss of central NE may directly impact brain health by interrupting neurotrophic factor signaling, exacerbating neuroinflammation, and altering regulation of innate and adaptive immune cells.
Highlights
Locus coeruleus (LC) degeneration and α-synuclein (α-syn) aggregation are among the most ubiquitous features of Parkinson’s disease (PD) (Chui et al, 1986; German et al, 1992; Zarow et al, 2003)
Brain regions affected in PD, including the LC, contain large protein-rich intracellular inclusions known as Lewy bodies (LB) or Lewy neurites (LN) accompanied by chronic inflammation and neuron loss
One study reports that treatment of T regulatory (Treg) with NE prior to transfer in an autoimmune arthritis mouse model rendered them pathological and worsened the disease (Harle et al, 2008)
Summary
Locus coeruleus (LC) degeneration and α-synuclein (α-syn) aggregation are among the most ubiquitous features of Parkinson’s disease (PD) (Chui et al, 1986; German et al, 1992; Zarow et al, 2003). LC degeneration and subsequent deficient brain NE may contribute to PD pathology by loss of normal immune cell modulation.
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