BACKGROUND AND PURPOSE: VRSs are the perivascular spaces surrounding the deep perforating arteries in the brain. Although VRS variations with age and disease pathologies have been reported previously, the radiologic characteristics of the VRS in relation to AD are poorly understood. This study investigated the prevalence, spatial distribution, and severity of the VRS in AD, MCI, and older adults who were CN. It also investigated the relationship of the VRS to white matter changes. MATERIALS AND METHODS: Structural MR imaging data were acquired from 158 participants (AD = 37, MCI = 71, CN = 50, mean age = 74.97 ± 7.20 years) who had undergone T1WI at 3T. The severity of VRS in the white matter, basal ganglia, hippocampus, and brain stem structures was evaluated by using a semiquantitative scale, adapted from existing rating scales. A VRS total score summarizing the subscales was calculated to assess the whole-brain VRSs. RESULTS: VRSs were observed in multiple brain regions of all participants, typically presented as <2-mm well-margined symmetric round-, oval- and linear-shaped hypointensities on T1WI. The VRS total score increased with leukoaraiosis, atrophy, and advanced age (P < .001). Individuals with AD and MCI showed greater levels of VRS than control subjects. The VRS total score discriminated individuals with AD and those who were CN with an accuracy of 0.79 (95% CI, 0.69–0.89). CONCLUSIONS: VRSs are common in older adults and are more severe in AD and MCI than in CN. Whether increased VRSs can be reliably used to aid in AD diagnosis warrants further investigation.

Background On average, cognition declines as people age, but improvement can also occur. Objective To evaluate the dynamics of age-related changes in brain structure and cognitive function in patients with mild Alzheimer's disease (AD) and mild cognitive impairment (MCI) and in healthy control (HC) older adults. Methods High-resolution 3-Tesla MRI and clinical data were obtained from the Alzheimer's Disease Neuroimaging Initiative in 187 subjects (a cohort aged 55–91 years; AD=43, MCI=84, HC=60). At 24 months, 151 people had clinical and 128 had MRI follow-up. Brain structure was assessed using the Medial Temporal Atrophy Scale (MTAS) and the Brain Atrophy and Lesion Index (BALI). Cognition was assessed using the Mini-Mental State Examination (MMSE) and the Alzheimer Disease Assessment Scale-cognitive subscale (ADAS-cog). Responsiveness was tested. Changes were analysed using a multistate dynamic model, adjusted for age, gender, ApoE4 genotype and vascular risk factors. Results Over 2 years, decline in brain structure and cognition predominated, each showing detectable effect sizes (Cohen's d=0.33 for MTAS, 0.32 for BALI, 0.41 for MMSE, 0.38 for ADAS-cog; standard response mean=0.71, 0.69, 0.50 and 0.47, respectively). Structural improvement was observed (10.2% in BALI and 0.8% in MTAS), as was cognitive improvement (23.2% MMSE, 27.2% ADAS-cog). Most people (66.7%) whose BALI score improved also improved in either the MMSE or ADAS-cog. No patient with MCI whose MTAS or BALI improved converted to AD. Conclusions Despite average decline in brain structure, improvement was observed and related to cognition and MCI–AD conversion. Ageing-related brain changes reflect a dynamic process.

Lung cancer is a malignancy with one of the highest incidence rates, and it is the leading cause of cancer‐related death. To gain further insights into the underlying mechanisms of tumor growth and metastasis, we investigated the role and expression of microRNAs in lung adenocarcinoma (LUAD). We discovered a significantly lower expression level of microRNA‐520c‐3p (miR‐520c‐3p) in LUAD tissues than in nontumor tissues. miR‐520c‐3p is known to regulate multiple biological functions and cellular behaviors. In this study, we show that AKT1 and AKT2 are key direct targets of miR‐520c‐3p, which are required for its biological roles in LUAD. Mechanistically, downregulation of miR‐520c‐3p in LUAD is due to DNA methylation of the miR‐520c‐3p promoter region. Conversely, the activity of the transcription factor Yin Yang 1 (YY1) results in the upregulation of miR‐520c‐3p. Taken together, our results reveal methylation/YY1/miR‐520c‐3p/AKT1/AKT2 as a molecular axis with a potent biological function and highlight miR‐520c‐3p as a novel potent tumor suppressor in LUAD.

Background: A brain atrophy and lesion index (BALI) based on high-field magnetic resonance imaging (MRI) has recently been validated to evaluate structural changes in the aging brain. The present study investigated the two-year progression of brain s

BACKGROUND AND PURPOSE: The Brain Atrophy and Lesion Index combines several common, aging-related structural brain changes and has been validated for high-field MR imaging. In this study, we evaluated measurement properties of the Brain Atrophy and Lesion Index by use of T1WI and T2WI at 1.5T and 3T MR imaging to comprehensively assess the usefulness of the lower field-strength testing. MATERIALS AND METHODS: Data were obtained from the Alzheimer9s Disease Neuroimaging Initiative. Images of subjects (n = 127) who had T1WI and T2WI at both 3T and 1.5T on the same day were evaluated, applying the Brain Atrophy and Lesion Index rating. Criterion and construct validity and interrater agreement were tested for each field strength and image type. RESULTS: Regarding reliability, the intraclass correlation coefficients for the Brain Atrophy and Lesion Index score were consistently high (>0.81) across image type and field strength. Regarding construct validity, the Brain Atrophy and Lesion Index score differed among diagnostic groups, being lowest in people without cognitive impairment and highest in those with Alzheimer disease (F > 5.14; P < .007). Brain Atrophy and Lesion Index scores correlated with age (r > 0.37, P < .001) and cognitive performance (r > 0.38, P < .001) and were associated with positive amyloid-β test (F > 3.96, P < .050). The T1WI and T2WI Brain Atrophy and Lesion Index scores were correlated (r > 0.93, P < .001), with the T2WI scores slightly greater than the T1WI scores (F > 4.25, P < .041). Regarding criterion validation of the 1.5T images, the 1.5T scores were highly correlated with the 3T Brain Atrophy and Lesion Index scores (r > 0.93, P < .001). CONCLUSIONS: The higher field and T2WI more sensitively detect subtle changes in the deep white matter and perivascular spaces in particular. Even so, 1.5T Brain Atrophy and Lesion Index scores are similar to those obtained by use of 3T images. The Brain Atrophy and Lesion Index may have use in quantifying the impact of dementia on brain structures.