Brain energy metabolic impairment is one of the main features of Alzheimer's disease (AD) and is considered an underlying factor involved in cognitive impairment. Therefore, brain energy metabolism may represent a new therapeutic target for AD medical interventions. Among nutrients providing energy, glucose, the primary energy source, cannot cross the blood-brain barrier freely without specific glucose transporters (GLUTs), which are essential for the maintenance of cerebral energy metabolism homeostasis. Several converging lines of evidence suggest that GLUT1 deficiency in mice leads to synapse reduction and dysregulation coupled with mitochondrial morphological changes. In this study, the results revealed that regular exercise (RE) decreased the expression of amyloid-␤ and phosphorylated tau by western blot, and enhanced the spatial learning and exploration ability of AD model mice as assessed by Morris water maze test. Mitochondrial cristae and edges were clear and intact, ATP production in the brain raised, the number of synapses increased, and GLUT1 and GLUT3 expression levels improved in the central nervous system (CNS) in AD model mice after RE. Changes in GLUT1 and GLUT3 expression at the protein level after RE are an important part of energy metabolic adaptation in AD model mice. Learning and memory improvement are highly associated with mitochondrial integrity and sufficient synapses in the CNS. This research suggests that increased brain energy metabolism attributed to RE exhibits promising therapeutic potential for AD.

Background: Physical exercise has been shown to improve cognitive and motor functions, promoting neurogenesis and demonstrating therapeutic benefits in neurodegenerative disorders. Nonetheless, it is crucial to investigate the cellular and molecular mechanisms by which this occurs. The study aimed to investigate and evaluate the effect of swimming exercise on the changes of mitochondrial proteins in the brains of rats with hypoxic ischemic encephalopathy (HIE). Methods: the vertical pole and Morris water maze tests were used to assess the animals’ motor and cognitive functions, and western blot and immunofluorescence of brain tissue were used to assess the biomarkers of mitochondrial apoptosis and cristae stability in response to exercise training. Four groups of rats were used: (1) sham sedentary group (SHAM, NT), (2) sham exercise training group (SHAM, T) (3) hypoxic ischemic encephalopathy sedentary group (HIE, NT), and (4) hypoxic ischemic encephalopathy exercise training group (HIE, T). Results: animals with HIE showed motor and cognitive deficits, as well as increased apoptotic protein expression. Exercise, on the other hand, improved motor and cognitive functions while also suppressing the expression of apoptotic proteins. Conclusions: By stabilizing the mitochondrial cristae and suppressing the apoptotic cascade, physical exercise provided neuroprotection in hypoxic ischemia-induced brain injury.

William Wordsworth, one of the greatest poets in England, is known as the poet of nature. His poems took on greater significance in English literature. The purpose of this essay is to study his source of forming such a lyrical style and the process he expressed his ideal in singing highly of the nature to show my respect towards him. Keywords Nature, Lyrical Style, RomanticismAt the turn of the 18th and the 19th centuries, romanticism came to be the new trend in English literature. William Wordsworth, the representative poet of Romanticism, whose poems took on greater significance, brought a totally new and fresh stream of air to the European literary field. Wordsworth, the glittering star, is always shinning in English literature. His whole life had a close connection with nature-the permanent subject sung highly by human being. Wordsworth was called by Shelly "Poet of nature". He, too, called himself "A Worshiper of Nature". He held a firm faith that nature could enlighten the kindheartedness and universal brotherhood of human being, and only exist in harmony with nature where man could get true happiness. In his poems of nature he printed beautiful pictures full of the creation by the mighty God-mountains, rocks, rivers and trees. All of them revealed the poets genuine love towards the nature, the fervent enthusiasm of pursuing the truth of life. The purpose of this essay is to study his source of forming such a lyrical style and the process he expressed his ideal in singing highly of the nature to show my respect towards him.Wordsworth's birth place was near to nature. Born in Cockermouth, just on the northern fringe of the English Lake district, he spent his childhood there. As a child, he often wandered among the fields and woods. At the age of 8, he was fed by one of his relatives who gave him simple food and shelter, but freedom of enjoying the nature. The Natural scenes and sounds gave his imagination wings and made him get to know the cottagers, shepherds, and solitary wanders that then entered his dreams and even his later poems. At the age of 14, Wordsworth

Monocarboxylates cannot cross the blood‐brain barrier freely to participate in brain energy metabolism. Specific monocarboxylate transporters (MCTs) are needed to cross cellular membranes. Monocarboxylate transporter 2 (MCT2) is a major monocarboxylate transporter encoded by the SLC16A7 gene. Recent studies reported that neurodegenerative diseases of the CNS, such as Alzheimer's disease (AD) and Parkinson's disease (PD), were related to energy metabolic impairment. MCT2 also plays an important role in energy metabolism in the CNS. To provide experimental evidence for future research on the role of MCT2 in the pathological process of CNS degenerative diseases, the distribution and density of MCT2 in different subregions of wild‐type mouse brain was examined using immunohistochemistry, western blot and immunogold post‐embedding electron microscopic techniques. The amount of MCT2 was higher in cerebellum than in cortex and hippocampus on western blots, and there was no statistical difference between cortex and hippocampus. Immunohistochemistry assay revealed the highest density of MCT2 in the CA3 of the hippocampus. The granular cell layer of the cerebellum contained more MCT2 than the molecular layer. The MCT2 density on the end feet of astrocytes of molecular layer was lower than in hippocampus, but the postsynaptic densities (PSDs) of asymmetric synapses in the molecular layer exhibited a high density using immunogold post‐embedding electron microscopic techniques.

Objective. To investigate the role of aberrant Dyrk1a expression in phosphorylation modification at the α-synuclein serine 129 (Ser129) site to analyze its molecular mechanism in mediating apoptosis of PD. Methods. The protein level of P-α-synuclein (Ser129), α-synuclein, Bcl-2, Bax, active caspase 3, GSK3β, PI3K, AKT, and cyclinD1 were detected. The mRNA transcript levels of Dyrk1a and DAT and protein levels of IL-1β, IL-6, COX-2, and TNF-α were detected. Results. P-α-synuclein (Ser129), α-synuclein, Bax, active caspase 3, GSK3β, and cyclinD1 expressions were decreased in Dyrk1a-AAV-ShRNA ( P  < 0.05), and Bcl-2, AKT, and PI3K expressions were increased ( P  < 0.05). Increased TH protein expression was shown in Dyrk1a-AAV-ShRNA ( P  < 0.05). Dyrk1a mRNA was decreased in the Dyrk1a-AAV-ShRNA group ( P  < 0.05), and DAT mRNA was increased ( P  < 0.05). IL-1β, IL-6, COX-2, and TNF-α protein levels were decreased in Dyrk1al-AAV-Sh-RNA ( P  < 0.05). Transcriptome sequencing showed that Fam220a, which was expected to activate STAT family protein binding activity and participate in the negative regulation of transcription through RNA polymerase II and protein dephosphorylation showed differentially upregulated expression. The untargeted metabolome showed that the major compounds in the Dyrk1a-AAV-ShRNA group were hormones and transmission mediators and the most metabolism-related pathways. Fam220a showed differentially upregulated expression, and differentially expressed genes were enriched for the neuroactive ligand-receptor interaction, vascular smooth muscle contraction, and melanogenesis-related pathways. Conclusion. Abnormal Dyrk1a expression can affect α-synuclein phosphorylation modifications, and dyrk1a knockdown activates the PI3K/AKT pathway and reduces dopaminergic neuron apoptosis. It provides a theoretical basis for the group to further investigate the molecular mechanism.