Abstract of recent abstracts:
Trehalose induces autophagy.
Autophagy induces neuronal repair.
Starvation induces autophagy.
Trehalose goes well with coffee and tea.
Quote: “Macroautophagy (here simply called autophagy) is a cellular housekeeping process that degrades and recycles long-lived proteins, large protein aggregates, and even entire organelles like mitochondria. The term autophagy is of Greek origin and translates literally as ‘the eating of oneself.’ ”
Many of the neurodegenerative diseases that afflict people are caused by intracytoplasmic aggregate-prone proteins. These include Parkinson disease, tauopathies, and polyglutamine expansion diseases such as Huntington disease. In Mendelian forms of these diseases, the mutations generally confer toxic novel functions on the relevant proteins. Thus, one potential strategy for dealing with these mutant proteins is to enhance their degradation. This can be achieved by up-regulating macroautophagy, which we will henceforth call autophagy. In this minireview, we will consider the reasons why autophagy up-regulation may be a powerful strategy for these diseases. In addition, we will consider some of the drugs and associated signaling pathways that can be used to induce autophagy with these therapeutic aims in mind.
Trehalose & autophagy vs. Parkinson’s disease,
Huntington’s disease, and prion infection
Overall, our study provides the first experimental evidence for the impact of autophagy in yet another type of neurodegenerative disease, namely prion disease.
— Note dosage: 1% trehalose in drinking water —
We have developed and characterized a mouse model of tauopathy with parkinsonism, overexpressing human mutated tau protein with deletion of parkin (PK–/–/TauVLW)….In this work, we tested if 1% trehalose in the drinking water reverts the PK?/?/TauVLW phenotype….the 3-week treatment with trehalose of 14-month-old PK–/–/TauVLW mice, at the limit of their life expectancy, improved the motor behavior and anxiety of these animals, and reduced their levels of phosphorylated tau and the number of murine β-amyloid plaques….Since trehalose is free of toxic effects at high concentrations, this study opens the way for clinical studies of the effects of trehalose in human tauopathies.
Autophagy is a nonspecific bulk degradation pathway for long-lived cytoplasmic proteins, protein complexes, or damaged organelles. This process is also a major degradation pathway for many aggregate-prone, disease-causing proteins associated with neurodegenerative disorders….We also report the growing list of new drugs/pathways that upregulate autophagy to enhance the clearance of this mutant protein, as autophagy upregulation may be a tractable strategy for the treatment of Huntington’s disease.
Autophagy, Alzheimer’s disease, and aging in general
This review is mainly focused in the discussion of evidence suggesting a clear association between mitochondrial dysfunction, autophagy impairment and amyloid-β accumulation in Alzheimer’s disease pathophysiology. The knowledge that autophagic insufficiency may compromise the cellular degradation mechanisms that may culminate in the progressive accumulation of dysfunctional mitochondria, aberrant protein aggregates buildup and lysosomal burden shield new insights to the way we address Alzheimer’s disease. In line with this knowledge an innovative window for new therapeutic strategies aimed to activate or ameliorate macroautophagy may be opened.
Recent studies have revealed that the same signaling factors regulate both aging and autophagocytosis, thus highlighting the role of autophagy in the regulation of aging and age-related degenerative diseases. Here, we examine in detail the interactions of the signaling network involving longevity factors SIRT1, mTOR, FoxO3, NF-kappaB and p53 in the regulation of autophagy. We discuss the possibility that these well-known stress resistance and longevity factors regulate the aging process via autophagy.
Trehalose: More than edible, it’s yummy
This paper contains a review of the history, natural occurrence, human consumption [e.g., in Japan], metabolism, manufacture, and the results of eight standardized animal safety studies using trehalose….trehalose is safe for use as an ingredient in consumer products when used in accordance with current Good Manufacturing Practices.
What if we could sweeten foods and beverages without sucrose (table sugar) and without chemical sugar substitutes (like aspartame or sucrolose)? What if there were a naturally occurring sugar that not only sweetens but enhances flavor? And what if that natural sugar was actually good for you? Introducing Trehalose (Tree-UH-lowz), an all-natural sugar now available for home use for the first time since its discovery over 175 years ago. Trehalose is sweet and energerizing!…As a sweetener, Trehalose does not interfere with natural flavors and does not produce a rapid rise in blood glucose seen with sucrose and other sugars. The enzyme that digests Trehalose is found primarily in the small intestine, which means it is not fully metabolized until 2 or 3 hours after digestion. This slow process may also be the key to sustained energy and endurance Trehalose appears to offer.
Trehalose: Basic Science Dept.
This review aims to highlight the changing perception of the role of trehalose over the last 10 years and to propose common mechanisms that may be involved in all the myriad ways in which trehalose stabilizes protein structures. These will take into account the structure of trehalose molecule and its interactions with its environment, and the explanations will focus on the role of trehalose in preventing protein denaturation.
Trehalose: Implausible Realities Dept.
Human primary fibroblasts expressing trehalose could be maintained in the dry state for up to five days. Fourier transform infrared spectroscopy indicated that dry, but viable, human cells contained no detectable water.
An afternoon update: Autophagy, lipids, and metabolic syndrome
Here we show a previously unknown function for autophagy in regulating intracellular lipid stores (macrolipophagy)….Decreased autophagy in the liver with ageing may contribute to hepatic lipid accumulation that occurs along with an increased incidence of the metabolic syndrome in aged humans. The ability of increased lipid content to impair autophagy also indicates that lipid accumulation could contribute to the decrease in autophagic function with ageing. Therapeutic strategies to increase autophagic function may therefore provide a new approach to prevent the metabolic syndrome and its associated pathologies.