Improvements of Motor Performances in the <i>Drosophila LRRK2</i> Loss-of-Function Model of Parkinson’s Disease: Effects of Dialyzed Leucocyte Extracts from Human Serum

• Main Authors: Andrea Diana, Maria Collu, Maria Antonietta Casu, Ignazia Mocci, Miguel Aguilar-Santelises, Maria Dolores Setzu
• Format: Article
• Language: English
• Published: MDPI AG 2020-01-01
• Series: Brain Sciences
• Subjects: <i>drosophila melanogaster</i>; <i>lrrk2</i> loss-of-function; parkinson’s disease; motor functions; human dialyzed leukocyte extract
• Online Access: https://www.mdpi.com/2076-3425/10/1/45

Within neurodegenerative syndromes, Parkinson&#8217;s disease (PD) is typically associated with its locomotor defects, sleep disturbances and related dopaminergic (DA) neuron loss. The fruit fly, <i>Drosophila melanogaster</i> (<i>D. melanogaster</i>), with leucine-rich repeat kinase 2 mutants (<i>LRRK2</i>) loss-of-function in the WD40 domain, provides mechanistic insights into corresponding human behaviour, possibly disclosing some physiopathologic features of PD in both genetic and sporadic forms. Moreover, several data support the boosting impact of innate and adaptive immunity pathways for driving the progression of PD. In this context, human dialyzable leukocyte extracts (DLE) have been extensively used to transfer antigen-specific information that influences the activity of various immune components, including inflammatory cytokines. Hence, the main goal of our study was to ascertain the therapeutic potential of DLE from male and female donors on <i>D. melanogaster LRRK2</i> loss-of-function, as compared to <i>D. melanogaster</i> wild-type (WT), in terms of rescuing physiological parameters, such as motor and climbing activities, which are severely compromised in the mutant flies. Finally, in search of the anatomical structures responsible for restored functions in parkinsonian-like mutant flies, we found a topographical correlation between improvement of locomotor performances and an increased number of dopaminergic neurons in selective areas of <i>LRRK2</i> mutant brains.