Efficacy of invasive and non-invasive methods for the treatment of Parkinson's disease: Nanodelivery and enriched environment.

Parkinson's disease (PD) is the second most common neurodegenerative disorder characterised by the loss of dopaminergic neurons in the substantia nigra pars compacta and the subsequent motor disability. The most frequently used treatments in clinics, such as L-DOPA, restore dopaminergic neurotransmission in the brain. However, these treatments are only symptomatic, have temporary efficacy, and produce side effects. Part of the side effects are related to the route of administration as the consumption of oral tablets leads to unspecific pulsatile activation of dopaminergic receptors. For this reason, it is necessary to not only find alternative treatments, but also to develop new administration systems with better security profiles. Nanoparticle delivery systems are new administration forms designed to reach the pharmacological target in a highly specific way, leading to better drug bioavailability, efficacy and safety. Some of these delivery systems have shown promising results in animal models of PD not only when dopaminergic drugs are administered, but even more when neurotrophic factors are released. These latter compounds promote maturation and survival of dopaminergic neurons and can be exogenously administered in the form of pharmacological therapy or endogenously generated by non-pharmacological methods. In this sense, experimental exposure to enriched environments, a non-invasive strategy based on the combination of social and inanimate stimuli, enhances the production of neurotrophic factors and produces a neuroprotective effect in parkinsonian animals. In this review, we will discuss new nanodelivery systems in PD with a special focus on therapies that increase the release of neurotrophic factors.

Enriched environment as a nonpharmacological neuroprotective strategy.

The structure and functions of the central nervous system are influenced by environmental stimuli, which also play an important role in brain diseases. Enriched environment (EE) consists of producing modifications in the environment of standard laboratory animals to induce an improvement in their biological conditions. This paradigm promotes transcriptional and translational effects that result in ameliorated motor, sensory, and cognitive stimulation. EE has been shown to enhance experience-dependent cellular plasticity and cognitive performance in animals housed under these conditions compared with animals housed under standard conditions. In addition, several studies claim that EE induces nerve repair by restoring functional activities through morphological, cellular, and molecular adaptations in the brain that have clinical relevance in neurological and psychiatric disorders. In fact, the effects of EE have been studied in different animal models of psychiatric and neurological diseases, such as Alzheimer's disease, Parkinson's disease, schizophrenia, ischemic brain injury, or traumatic brain injury, delaying the onset and progression of a wide variety of symptoms of these disorders. In this review, we analyze the action of EE focused on diseases of the central nervous system and the translation to humans to develop a bridge to its application.

Pectic galactan affects cell wall architecture during secondary cell wall deposition.

MAIN CONCLUSION: ß-(1,4)-galactan determines the interactions between different matrix polysaccharides and cellulose during the cessation of cell elongation. Despite recent advances regarding the role of pectic ß-(1,4)-galactan neutral side chains in primary cell wall remodelling during growth and cell elongation, little is known about the specific function of this polymer in other developmental processes. We have used transgenic Arabidopsis plants overproducing chickpea ßI-Gal ß-galactosidase under the 35S CaMV promoter (35S::ßI-Gal) with reduced galactan levels in the basal non-elongating floral stem internodes to gain insight into the role of ß-(1,4)-galactan in cell wall architecture during the cessation of elongation and the beginning of secondary growth. The loss of galactan mediated by ßI-Gal in 35S::ßI-Gal plants is accompanied by a reduction in the levels of KOH-extracted xyloglucan and an increase in the levels of xyloglucan released by a cellulose-specific endoglucanase. These variations in cellulose-xyloglucan interactions cause an altered xylan and mannan deposition in the cell wall that in turn results in a deficient lignin deposition. Considering these results, we can state that ß-(1,4)-galactan plays a key structural role in the correct organization of the different domains of the cell wall during the cessation of growth and the early events of secondary cell wall development. These findings reinforce the notion that there is a mutual dependence between the different polysaccharides and lignin polymers to form an organized and functional cell wall.