Trehalase localization in the cerebral cortex, hippocampus and cerebellum of mouse brains

Halbe, Luisa; Rami, Abdelhaq

doi:10.1016/j.jare.2019.01.009

Cited by 13 publications

(4 citation statements)

References 46 publications

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“…Many active substances with neuroprotective activities remain to be evaluated for the PLGA NP approach to improve their brain delivery [ 101 , 102 , 103 , 104 , 105 , 106 , 107 , 108 , 109 , 110 , 111 , 112 , 113 , 114 , 115 ]. Some of them, such as trehalose, exhort numerous properties ranging from anti-inflammatory to anti-oxidant, which can potentially be applied for out of current applications and NDDs treatment.…”

Section: New Candidates For Plga Nps Vectorizationmentioning

confidence: 99%

“…Trehalose treatment reduced the level of toxic protein aggregates, which in turn improve behavioral symptoms and survival in animal models of NDDs including AD [ 106 ], PD [ 107 , 108 ], and HD [ 109 ]. However, trehalose can be cleaved by trehalase, an enzyme observed in different mammalian organs [ 110 ]. Therefore, PLGA NPs could be interesting candidates to protect trehalose from degradation and improve its bioavailability.…”

Section: New Candidates For Plga Nps Vectorizationmentioning

confidence: 99%

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PLGA-Based Nanoparticles for Neuroprotective Drug Delivery in Neurodegenerative Diseases

et al. 2021

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Treatment of neurodegenerative diseases has become one of the most challenging topics of the last decades due to their prevalence and increasing societal cost. The crucial point of the non-invasive therapeutic strategy for neurological disorder treatment relies on the drugs’ passage through the blood-brain barrier (BBB). Indeed, this biological barrier is involved in cerebral vascular homeostasis by its tight junctions, for example. One way to overcome this limit and deliver neuroprotective substances in the brain relies on nanotechnology-based approaches. Poly(lactic-co-glycolic acid) nanoparticles (PLGA NPs) are biocompatible, non-toxic, and provide many benefits, including improved drug solubility, protection against enzymatic digestion, increased targeting efficiency, and enhanced cellular internalization. This review will present an overview of the latest findings and advances in the PLGA NP-based approach for neuroprotective drug delivery in the case of neurodegenerative disease treatment (i.e., Alzheimer’s, Parkinson’s, Huntington’s diseases, Amyotrophic Lateral, and Multiple Sclerosis).

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Section: New Candidates For Plga Nps Vectorizationmentioning

confidence: 99%

Section: New Candidates For Plga Nps Vectorizationmentioning

confidence: 99%

PLGA-Based Nanoparticles for Neuroprotective Drug Delivery in Neurodegenerative Diseases

et al. 2021

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“…Trehalose is a disaccharide found in bacteria, yeast, insects, fungi, and plants but not in mammals [ 1 , 2 ]. Two glucose molecules are linked via an alpha-glycosidic linkage, providing heat and pH resistance [ 3 ].…”

Section: Introductionmentioning

confidence: 99%

“…The degrading enzyme trehalase cleaves trehalose and provides glucose as an energy resource in microorganisms such as mycobacteria but not in mammalians [ 1 , 3 ]. Nevertheless, trehalase was also found in the brain of mice [ 2 ] and in the gastrointestinal tract of mice and humans [ 4 ], likely originating in part from the gut microbiome [ 5 , 6 , 7 ]. The bioavailability of ingested trehalose is low [ 8 , 9 ] and may depend on bacteria colonization [ 10 ].…”

Section: Introductionmentioning

confidence: 99%

Trehalose Reduces Nerve Injury Induced Nociception in Mice but Negatively Affects Alertness

et al. 2021

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Trehalose, a sugar from fungi, mimics starvation due to a block of glucose transport and induces Transcription Factor EB- mediated autophagy, likely supported by the upregulation of progranulin. The pro-autophagy effects help to remove pathological proteins and thereby prevent neurodegenerative diseases such as Alzheimer’s disease. Enhancing autophagy also contributes to the resolution of neuropathic pain in mice. Therefore, we here assessed the effects of continuous trehalose administration via drinking water using the mouse Spared Nerve Injury model of neuropathic pain. Trehalose had no effect on drinking, feeding, voluntary wheel running, motor coordination, locomotion, and open field, elevated plus maze, and Barnes Maze behavior, showing that it was well tolerated. However, trehalose reduced nerve injury-evoked nociceptive mechanical and thermal hypersensitivity as compared to vehicle. Trehalose had no effect on calcium currents in primary somatosensory neurons, pointing to central mechanisms of the antinociceptive effects. In IntelliCages, trehalose-treated mice showed reduced activity, in particular, a low frequency of nosepokes, which was associated with a reduced proportion of correct trials and flat learning curves in place preference learning tasks. Mice failed to switch corner preferences and stuck to spontaneously preferred corners. The behavior in IntelliCages is suggestive of sedative effects as a “side effect” of a continuous protracted trehalose treatment, leading to impairment of learning flexibility. Hence, trehalose diet supplements might reduce chronic pain but likely at the expense of alertness.

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Trehalose against Alzheimer's Disease: Insights into a Potential Therapy

et al. 2020

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Trehalose is a natural disaccharide with a remarkable ability to stabilize biomolecules. In recent years, trehalose has received growing attention as a neuroprotective molecule and has been tested in experimental models for different neurodegenerative diseases. Although the underlying neuroprotective mechanism of trehalose's action is unclear, one of the most important hypotheses is autophagy induction. The chaperone‐like activity of trehalose and the ability to modulate inflammatory responses has also been reported. There is compelling evidence that the dysfunction of autophagy and aggregation of misfolded proteins contribute to the pathogenesis of Alzheimer's disease (AD) and other neurodegenerative disorders. Therefore, given the linking between trehalose and autophagy induction, it appears to be a promising therapy for AD. Herein, the published studies concerning the use of trehalose as a potential therapy for AD are summarized, providing a rationale for applying trehalose to reduce Alzheimer's pathology.

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Trehalase localization in the cerebral cortex, hippocampus and cerebellum of mouse brains

Abstract: Graphical abstract

Cited by 13 publications

References 46 publications

PLGA-Based Nanoparticles for Neuroprotective Drug Delivery in Neurodegenerative Diseases

PLGA-Based Nanoparticles for Neuroprotective Drug Delivery in Neurodegenerative Diseases

Trehalose Reduces Nerve Injury Induced Nociception in Mice but Negatively Affects Alertness

Trehalose against Alzheimer's Disease: Insights into a Potential Therapy

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