Vanillin, a Newly Discovered Autotoxic Substance in Long-Term Potato Continuous Cropping Soil, Inhibits Plant Growth by Decreasing the Root Auxin Content and Reducing Adventitious Root Numbers.

Phenolic acids are known to reduce root biomass and hinder plant development, but it is unclear how they affect potato root traits. Over a 10 year field experiment, we found a negative correlation between the potato yield and continuous cropping years. The substantial reduction in adventitious root (AR) numbers was found to be primarily inhibited by soil vanillin accumulation. The study also found that vanillin had a more pronounced inhibitory effect on the potato yield than commonly reported ferulic acid and p-hydroxybenzoic acid. The decrease in yield was attributed to the reduction of root indole-3-acetic acid (IAA) content, which impeded the formation of AR. Exogenous IAA was found to increase the root IAA content and stimulate AR formation under vanillin stress, ultimately leading to an increase in the potato yield. This study provides valuable insights into potential strategies for the degradation of autotoxic substances and breeding of potato cultivars with enhanced resistance to autotoxicity.

Effects of different altitudes on the structure and properties of potato starch.

The main element influencing the quality of potato starch is the environment. To investigate the effects of different altitude cultivation locations on the molecular structure and physicochemical properties of starch, two potato varieties, Jiusen No.1 B1 and Qingshu No.9 B2, were planted in three different altitude zones: A1 at low altitude (Chongzhou 450 m), A2 at middle altitude (Xichang 2800 m), and A3 at high altitude (Litang 3650 m). The results showed that the average volume, number, surface area diameter, average branched polymerization degree, crystallinity, and gelatinization temperature of two potato granules in high altitude areas were significantly lower than those in middle and low altitude areas were, and the gelatinization performance of potato starch was affected according to the correlation of starch structure characteristics. Potato starch with more short-branched chains and less long branched chains resulted in a lower gelatinization temperature in high altitude areas. The results showed that Jiusen No. 1 and Qingshu No. 9 were mainly affected by accumulated radiation and accumulated rainfall in Litang, a high altitude area, and by effective accumulated temperature in Xichang, a middle altitude area. This study quantified the influence of meteorological factors on the main starch quality of potato tubers. The results can be used as a theoretical basis for the scientific planting of high-quality potatoes.

Adiponectin alleviated Alzheimer-like pathologies via autophagy-lysosomal activation.

Adiponectin (APN) deficiency has also been associated with Alzheimer-like pathologies. Recent studies have illuminated the importance of APN signaling in reducing Aß accumulation, and the Aß elimination mechanism remains rudimentary. Therefore, we aimed to elucidate the APN role in reducing Aß accumulation and its associated abnormalities by targeting autophagy and lysosomal protein changes. To assess, we performed a combined pharmacological and genetic approach while using preclinical models and human samples. Our results demonstrated that the APN level significantly diminished in the plasma of patients with dementia and 5xFAD mice (6 months old), which positively correlated with Mini-Mental State Examination (MMSE), and negatively correlated with Clinical Dementia Rating (CDR), respectively. APN deficiency accelerated cognitive impairment, Aß deposition, and neuroinflammation in 5xFAD mice (5xFAD*APN KO), which was significantly rescued by AdipoRon (AR) treatment. Furthermore, AR treatment also markedly reduced Aß deposition and attenuated neuroinflammation in APP/PS1 mice without altering APP expression and processing. Interestingly, AR treatment triggered autophagy by mediating AMPK-mTOR pathway signaling. Most importantly, APN deficiency dysregulated lysosomal enzymes level, which was recovered by AR administration. We further validated these changes by proteomic analysis. These findings reveal that APN is the negative regulator of Aß deposition and its associated pathophysiologies. To eliminate Aß both extra- and intracellular deposition, APN contributes via the autophagic/lysosomal pathway. It presents a therapeutic avenue for AD therapy by targeting autophagic and lysosomal signaling.

Manganese exposure causes movement deficit and changes in the protein profile of the external globus pallidus in Sprague Dawley rats.

Manganese (Mn) is required for normal brain development and function. Excess Mn may trigger a parkinsonian movement disorder but the underlying mechanisms are incompletely understood. We explored changes in the brain proteomic profile and movement behavior of adult Sprague Dawley (SD) rats systemically treated with or without 1.0 mg/mL MnCl2 for 3 months. Mn treatment significantly increased the concentration of protein-bound Mn in the external globus pallidus (GP), as demonstrated by inductively coupled plasma mass spectrometry. Behavioral study showed that Mn treatment induced movement deficits, especially of skilled movement. Proteome analysis by two-dimensional fluorescence difference gel electrophoresis coupled with mass spectrometry revealed 13 differentially expressed proteins in the GP of Mn-treated versus Mn-untreated SD rats. The differentially expressed proteins were mostly involved in glycolysis, metabolic pathways, and response to hypoxia. Selected pathway class analysis of differentially expressed GP proteins, which included phosphoglycerate mutase 1 (PGAM1), primarily identified enrichment in glycolytic process and innate immune response. In conclusion, perturbation of brain energy production and innate immune response, in which PGAM1 has key roles, may contribute to the movement disorder associated with Mn neurotoxicity.

Loganin substantially ameliorates molecular deficits, pathologies and cognitive impairment in a mouse model of Alzheimer's disease.

Alzheimer's disease (AD) is the most common age-related neurodegenerative disease threatening the health of the elderly, but the available therapeutic and preventive drugs remain suboptimal. Loganin, an iridoid glycoside extracted from Cornus officinalis, is reported to have anti-inflammatory and memory-enhancing properties. This study is aimed to explore the influence of loganin on cognitive function in 3xTg-AD mice and the underlying mechanism associated with its neuroprotection. According to the results of behavioral tests, we found that administration of loganin could significantly alleviate anxiety behavior and improve memory deficits of 3xTg-AD mice. Furthermore, immunohistochemical analysis displayed that there were decreased Aß deposition in the hippocampus and cortex of 3xTg-AD mice treated with loganin compared with the control mice. Importantly, the Aß-related pathological change was mainly involved in altering APP expression and processing. And loganin was also found to reduce the levels of phosphorylated tau (i.e. pTauS396 and pTauS262) in 3xTg-AD mice. By performing 2D-DIGE combined with MALDI-TOF-MS/MS, we revealed 28 differentially expressed proteins in the 3xTg-AD mice treated with loganin compared with the control mice. Notably, 10 proteins largely involved in energy metabolism, synaptic proteins, inflammatory response, and ATP binding were simultaneously detected in 3xTg-AD mice compared to WT mice. The abnormal changes of energy metabolism (PAGM1 and ENO1), synaptic proteins (SYN2 and Cplx2), inflammatory response (1433Z) were verified by western blot. Overall, our study suggested that loganin could be used as a feasible candidate drug to ameliorate molecular deficits, pathologies and cognitive impairment for prevention and treatment of AD.

Low-Dose Copper Exposure Exacerbates Depression-Like Behavior in ApoE4 Transgenic Mice.

Depression is one of the most common neuropsychiatric disorders. Although the pathogenesis of depression is still unknown, environmental risk factors and genetics are implicated. Copper (Cu), a cofactor of multiple enzymes, is involved in regulating depression-related processes. Depressed patients carrying the apolipoprotein ε4 allele display more severe depressive symptoms, indicating that ApoE4 is closely associated with an increased risk of depression. The study explored the effect of low-dose Cu exposure and ApoE4 on depression-like behavior of mice and further investigates the possible mechanisms. The ApoE4 mice and wild-type (WT) mice were treated with 0.13 ppm CuCl2 for 4 months. After the treatment, ApoE4 mice displayed obvious depression-like behavior compared with the WT mice, and Cu exposure further exacerbated the depression-like behavior of ApoE4 mice. There was no significant difference in anxiety behavior and memory behavior. Proteomic analysis revealed that the differentially expressed proteins between Cu-exposed and nonexposed ApoE4 mice were mainly involved in the Ras signaling pathway, protein export, axon guidance, serotonergic synapse, GABAergic synapse, and dopaminergic synapse. Among these differentially expressed proteins, immune response and synaptic function are highly correlated. Representative protein expression changes are quantified by western blot, showing consistent results as determined by proteomic analysis. Hippocampal astrocytes and microglia were increased in Cu-exposed ApoE4 mice, suggesting that neuroglial cells played an important role in the pathogenesis of depression. Taken together, our study demonstrated that Cu exposure exacerbates depression-like behavior of ApoE4 mice and the mechanisms may involve the dysregulation of synaptic function and immune response and overactivation of neuroinflammation.