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

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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. ARTICLE HISTORY

Background Cerebral autosomal‐dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a cerebrovascular disease that is closely related to the NOTCH3 gene. Recurrent ischemic stroke, progressive cognitive dysfunction, and mental symptoms are the main clinical manifestations, whereas symptomatic intracranial hemorrhage is rare. Methods We detected a heterozygous mutation of c.1759C>T in exon 11 of the NOTCH3 gene that caused recurrent intracranial hemorrhage in CADASIL. Results Second‐generation sequencing of a sample of the patient's genome revealed a heterozygous mutation of c.1759C>T in exon 11 of NOTCH3 , which resulted in amino acid changes (p.R587C). This variation may be rated as a CADASIL clinical variation. Conclusion The discovery of this mutation site provides an important theoretical basis for a gene‐based diagnosis and treatment of recurrent intracranial hemorrhage.

Autosomal-dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a monogenic inherited cerebrovascular disease. The disease is caused by the mutations in NOTCH3 on chromosome 19. 1,2 CADASIL usually starts in the middle age, which is different from the traditional cerebrovascular disease, and it usually has no clear high-risk factors for cerebrovascular disease, with recurrent stroke as the main manifestation, which can be accompanied by cognitive impairment, dementia, mental and emotional disorders, and migraine with aura. 3 The presence of granular osmiophilic material (GOM) in close proximity to smooth muscle cells, pericytes, and endothelial cells is critical for the diagnosis of CADASIL. 4,5 Analysis of all the exons of the NOTCH3 gene is crucial to determine the mutation that causes the pathology. 6,7 The NOTCH3 gene, located on chromosome 19p13, encodes a single-pass transmembrane receptor, which is composed of a large extracellular domain (ECD) with 34 tandem epidermal growth factor-like (EGF) repeats encoded by exons 2-24, where NOTCH3 mutations are commonly found, a transmembrane domain, and an intracellular domain (ICD). [8][9][10] In all, 33 exons and 2321 amino acids constitute NOTCH3. 11 CADASIL is caused by the presence of only one mutation in one of the two alleles of NOTCH3 because pathogenic mutations are dominant in this disease. 12

Hereditary spastic paraplegia (HSP), also known as familial spastic paraplegia, is a rare familial hereditary neurodegenerative disease with a morbidity rate of 1.2-9.6 per 100,000 population. The genetic patterns of this disease include autosomal dominant inheritance, autosomal recessive inheritance, and X-linked recessive inheritance. 1 Although more than 50 causative genes have been identified, 2 the pathogenesis of HSP remains unclear. The pathological changes in HSP, such as bilateral corticospinal tract axonal degeneration and demyelination, are mainly seen in the spinal cord, particularly in the thoracic spinal cord. HSP is characterized by chronic progressive weakness and spastic lower limb paralysis. Optic atrophy, retinitis pigmentosa, extrapyramidal symptoms, cerebellar ataxia, sensory impairment, dementia, mental retardation, hearing loss, muscle atrophy, and autonomic nerve dysfunction may be present. Independent mutations in multiple genes can cause HSP; thus, the diagnosis and treatment of HSP are challenging. Therefore, further advancements in HSP gene mapping will be beneficial for the diagnosis and development of effective treatments based on genetic characteristics.In this study, we found a new mutation at the proline-rich transmembrane protein 2 (PRRT2) locus using second-generation sequencing. This mutation caused familial HSP with peripheral neuropathy.