Human α-synuclein overexpression upregulates SKOR1 in a rat model of simulated nigrostriatal ageing.

Parkinson's disease (PD) is characterised by progressive loss of dopaminergic (DA) neurons from the substantia nigra (SN) and α-synuclein (αSyn) accumulation. Age is the biggest risk factor for PD and may create a vulnerable pre-parkinsonian state, but the drivers of this association are unclear. It is known that ageing increases αSyn expression in DA neurons and that this may alter molecular processes that are central to maintaining nigrostriatal integrity.

STRAP and NME1 Mediate the Neurite Growth-Promoting Effects of the Neurotrophic Factor GDF5.

Loss of midbrain dopaminergic (mDA) neurons and their axons is central to Parkinson's disease (PD). Growth differentiation factor (GDF)5 is a potential neurotrophic factor for PD therapy. However, the molecular mediators of its neurotrophic action are unknown.

Time-course of striatal Toll-like receptor expression in neurotoxic, environmental and inflammatory rat models of Parkinson's disease.

Because Toll-like receptors (TLRs) are emerging as potential targets for anti-inflammatory intervention in neurodegenerative diseases, the aim of this study was to characterise the time-course of TLR expression in neurotoxic, environmental and inflammatory Parkinson's disease models. Male Sprague Dawley rats were given intra-striatal injections of 6-hydroxydopamine (10μg), rotenone (1.25μg), LPS (10μg) or Poly I:C (20μg) and were sacrificed on Days 1, 4, 14 and 28 post surgery.

Upregulation of the cannabinoid CB2 receptor in environmental and viral inflammation-driven rat models of Parkinson's disease.

In recent years, it has become evident that Parkinson's disease is associated with a self-sustaining cycle of neuroinflammation and neurodegeneration, with dying neurons activating microglia, which, once activated, can release several factors that kill further neurons. One emerging pharmacological target that has the potential to break this cycle is the microglial CB2 receptor which, when activated, can suppress microglial activity and reduce their neurotoxicity. However, very little is known about CB2 receptor expression in animal models of Parkinson's disease which is essential for valid preclinical assessment of the anti-Parkinsonian efficacy of drugs targeting the CB2 receptor.

Differential upregulation of the cannabinoid CB₂ receptor in neurotoxic and inflammation-driven rat models of Parkinson's disease.

The cannabinoid CB2 receptor has recently emerged as a potential anti-inflammatory target to break the self-sustaining cycle of neuroinflammation and neurodegeneration that is associated with neurodegenerative diseases. However, in order to facilitate the development of cannabinoid drugs for neurodegenerative disease, the changes that occur in the endocannabinoid system in response to different neurodegenerative triggers needs to be elucidated. Therefore, the aim of this study was to investigate and compare the changes that occur in the endocannabinoid system in neurotoxic and inflammation-driven models of Parkinson's disease.