Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by the accumulation of β-amyloid peptide 1-42 and phosphorylation of tau protein in the brain. Thus far, the transfer mechanism of these cytotoxic proteins between nerve cells remains unclear. Recent studies have shown that nanoscale extracellular vesicles (exosomes) originating from cells may play important roles in this transfer process. In addition, several genetic materials and proteins are also involved in intercellular communication by the secretion of the exosomes. That proposes novel avenues for early diagnosis and biological treatment in AD, based on exosome detection and intervention. In this review, exosome-related pathways of cytotoxic protein intercellular transfer in AD, and the effect of membrane proteins on exosomes targeting cells are first introduced. The advances in exosome-related biomarker detection in AD are summarized. Finally, the advantages and challenges of reducing cytotoxic protein accumulation via exosomal intervention for AD treatment are discussed. It is envisaged that future research in exosomes may well provide new insights into the pathogenesis, diagnosis, and treatment of AD.
The complete nucleotide sequence of the sugar beet (Beta vulgaris ssp. vulgaris) chloroplast genome (cpDNA) was determined in this study. The cpDNA was 149,637 bp in length, containing a pair of 24,439 bp inverted repeat regions (IR), which were separated by small and large single copy regions (SSC and LSC) of 17,701 and 83,057 bp, respectively. 53.4% of the sugar beet cpDNA consisted of gene coding regions (protein coding and RNA genes). The gene content and relative positions of 113 individual genes (79 protein encoding genes, 30 tRNA genes, 4 rRNA genes) were almost identical to those of tobacco cpDNA. The overall AT contents of the sugar beet cpDNA were 63.6% and in the LSC, SSC and IR regions were 65.9%, 70.8% and 57.8%, respectively. Fifteen genes contained one intron, while three genes had two introns.
Cerebral small vessel disease (CSVD) refers to lesions of the cerebral arterioles, venules, and capillaries caused by various causes. 1 Clinical manifestations of this type of disease are cognitive decline, abnormal gait, decreased executive function, mental symptoms, etc. 2 CSVD can be divided into sporadic and hereditary. Sporadic CSVD is mainly related to age, hypertension, diabetes, smoking, and other risk factors. 3 Hereditary CSVD accounts for approximately 5% of all cerebrovascular diseases caused by gene mutations, including cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), cerebral autosomal recessive
The complete mitochondrial genome of Amblyomma testudinarium is reported for the first time in this study. Its entire mitogenome is 14,760 bp in length, contained 13 protein-coding genes, 2 ribosomal RNA genes, 22 transfer RNA genes, and 2 non-coding regions. The phylogenetic analysis by Bayesian inference method show that A. testudinarium and the others of genus Amblyomma are in the same clade, indicating that A. testudinarium belongs to the genus Amblyomma.
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