Alzheimer's disease (AD) is the most common cause of dementia. Despite this, clear pathophysiology for AD has not been confirmed, and effective treatments are still not available. As AD results in a complex disease process for cognitive decline, various theories have been suggested as the cause of AD. Recently, cerebral small vessel disease (SVD) has been suggested to contribute to the pathogenesis of AD, as well as contributing to vascular dementia. Cerebral SVD refers to a varied group of diseases that affect cerebral small arteries and microvessels. These can be seen as white matter hyperintensities, cerebral microbleeds, and lacunes on magnetic resonance imaging. Data from epidemiological and clinical-pathological studies have found evidence of the relationship between cerebral SVD and AD. This review aims to discuss the complex relationship between cerebral SVD and AD. Recent reports that evaluate the association between these diseases will be reviewed.

Cerebrovascular disease is a potential risk factor for Alzheimer's disease (AD). Although acute cerebral hypoperfusion causes neuronal necrosis and infarction, chronic cerebral hypoperfusion induces apoptosis in neurons, but its effects on the cognitive impairment are not clear. The purpose of this study was to evaluate the effects of chronic cerebral hypoperfusion on AD pathology and cerebral glucose metabolism. A model of chronic cerebral hypoperfusion was established by ligating the common carotid arteries bilaterally in adult male rats (CAL group). Sham-operated rats underwent the same procedures without artery ligation (control group). At 12 weeks after ligation, expression levels of amyloid-β (Aβ) and hyperphosphorylated tau (p-tau), as well as the regional cerebral glucose metabolism, were evaluated using Western blots and positron emission tomography with fluorine-18 fluorodeoxyglucose, respectively. The expression levels of Aβ in the frontal cortex and hippocampus and of p-tau in the temporal cortex were significantly higher in the CAL group than those in the control group. The cerebral glucose metabolism of the amygdala, entorhinal cortex, and hippocampus was significantly decreased in the CAL group compared to that in the control. These results suggest that chronic cerebral hypoperfusion can induce AD pathology and may play a significant role in AD development.

The visceral adipose tissue (VAT) has been recognized as an endocrine organ, and VAT dysfunction could be a risk factor for Alzheimer’s disease (AD). We aimed to evaluate the association of VAT metabolism with AD pathology. This cross-sectional study included 54 older subjects with cognitive impairment who underwent 2-deoxy-2-[fluorine-18]-fluoro-D-glucose (¹⁸F-FDG) torso positron emission tomography (PET) and ¹⁸F-florbetaben brain PET. ¹⁸F-FDG uptake in VAT on ¹⁸F-FDG PET images was used as a marker of VAT metabolism, and subjects were classified into high and low VAT metabolism groups. A voxel-based analysis revealed that the high VAT metabolism group exhibited a significantly higher cerebral amyloid-β (Aβ) burden than the low VAT metabolism group. In the volume-of-interest analysis, multiple linear regression analyses with adjustment for age, sex, and white matter hyperintensity volume revealed that ¹⁸F-FDG uptake in VAT was significantly associated with the cerebral Aβ burden (β = 0.359, p = 0.007). In conclusion, VAT metabolism was associated with AD pathology in older subjects. Our findings suggest that VAT dysfunction could contribute to AD development.

The low sensitivity of F-18 fluorodeoxyglucose (FDG) positron emission tomography/computed tomography (PET/CT) for the evaluation of metastatic lymph nodes (LNs) is mainly due to the partial volume effect in patients with rectal cancer. This retrospective study evaluated the diagnostic accuracy of F-18 FDG PET/CT with optimal cut-off values of the maximum standardized uptake value (SUVmax), according to LN size, for the evaluation of regional LN in rectal cancer patients. This study included 176 patients with rectal cancer who underwent F-18 FDG PET/CT for initial staging. Patients were classified based on the long-axis diameter of the regional LN on CT images as small (≤ 7 mm; n = 118) and large (> 7 mm; n = 58) LN groups. The optimal cut-off value of SUVmax was determined for each group, using receiver operating characteristic curve analysis. Areas under the curve (AUC) were compared by C-statistics using two methods: the cut-off value of SUVmax optimized according to LN size, and a fixed SUVmax cut-off value of 2.5. The optimal cut-off values of SUVmax for the small and large LN groups were 1.1, and 2.1, respectively. The sensitivity, specificity, and accuracy of F-18 FDG PET/CT using the optimal cut-off values were 90.6, 70.9, and 76.3% in the small LN group, and 68.6, 78.3, and 72.4% in the large LN group. The sensitivity, specificity, and accuracy of F-18 FDG PET/CT using the fixed cut-off value were 18.8, 100, and 78.0% in the small LN group, and 51.4, 87.0, and 65.5% in the large LN group. The AUC was significantly higher using the optimal cut-off values than the fixed cut-off value (0.808 vs. 0.594, p = 0.005) in the small LN group, but not in the large LN group (0.734 vs. 0.692, p = 0.429). Application of the lower cut-off value of SUVmax improves the diagnostic performance of F-18 FDG PET/CT for the evaluation of small regional LNs in patients with rectal cancer.

Alzheimer’s disease (AD) is a neurodegenerative disease characterized by the deposition of amyloid-β peptide (Aβ) in diffuse and neuritic plaques. Previous research has suggested that certain vitamins may prevent this process. In the present study, we evaluated the relationship between vitamin intake and cerebral Aβ burden in patients with cognitive impairment. This study included 19 patients with subjective cognitive impairment and 30 patients with mild cognitive impairment. All patients underwent brain MRI and 18F-florbetaben positron emission tomography. The Food Frequency Questionnaire was used to evaluate dietary intake of the 15 vitamins. Intake of vitamin B6 (p = 0.027), vitamin K (p = 0.042), vitamin A (p = 0.063), riboflavin (p = 0.063), β-carotene (p = 0.081), pantothenic acid (p = 0.092), and niacin (p = 0.097) was higher in the Aβ-positive group than in the Aβ-negative group. Multivariate linear regression analysis revealed that pantothenic acid intake was an independent determinant of cerebral Aβ burden (β = 0.287, p = 0.029). No significant correlations were observed between cerebral Aβ burden and the intake of other vitamins. Our findings demonstrated that pantothenic acid intake may be associated with increased cerebral Aβ burden in patients with cognitive impairment. These results may offer insight into potential strategies for AD prevention.

White matter lesions (WMLs), detected as hyperintensities on T2-weighted MRI, represent small vessel disease in the brain and are considered a potential risk factor for memory and cognitive impairment in older adults. The purpose of this study was to evaluate the association between WMLs and cerebral amyloid-β (Aβ) burden in patients with cognitive impairment. A total of 83 patients with cognitive impairment, who underwent brain MRI and F-18 florbetaben PET, were included prospectively: 19 patients were cognitively unimpaired, 30 exhibited mild cognitive impairment (MCI), and 34 exhibited dementia. The Fazekas scale was used to quantify WMLs on T2-weighted brain MR images. Cerebral Aβ burden was quantitatively estimated using volume-of-interest analysis. Differences in cerebral Aβ burden were evaluated between low-WML (Fazekas scale ≤1) and high-WML (Fazekas scale ≥2) groups. The relationship between the Fazekas rating and cerebral Aβ burden was evaluated using linear regression analysis after adjusting for age and sex. In the overall cohort, the high-WML group exhibited significantly higher Aβ burden compared with the low-WML group (P = 0.011) and cerebral Aβ burden was positively correlated with Fazekas rating (β = 0.299, P = 0.006). In patients with MCI, the high-WML group exhibited significantly higher Aβ burden compared with the low-WML group (P = 0.019) and cerebral Aβ burden was positively correlated with Fazekas rating (β = 0.517, P = 0.003). The presence of WMLs was associated with cerebral Aβ burden in patients with MCI. Our findings suggest that small vessel disease in the brain is related to Alzheimer’s disease pathology.