Naoyuki Sato 교수

The incidence of dementia is increasing at an alarming rate, and has become a major public health concern. Alzheimer disease (AD) is the most common form of dementia and is characterized by progressive cognitive impairment. In addition to classical neuropathological features such as amyloid plaques and neurofibrillary tangles (NFT), accumulation of activated immune cells has been documented in the AD brain, suggesting a contribution of neuroinflammation in the pathogenesis of AD. Besides cogniti

Diabetes is a risk factor for Alzheimer disease (AD). Apolipoprotein E (ApoE) and several genes related to AD have recently been identified by genome-wide association studies (GWAS) as being closely linked to lipid metabolism. Lipid metabolism and glucose-energy metabolism are closely related. Here, we review the emerging evidence regarding the roles of lipid and glucose metabolism in the modulation of β-amyloid, tau, and neurodegeneration during the pathogenesis of AD. Disruption of homeostasis

The incidence of Alzheimer disease (AD) and diabetes mellitus (DM) is increasing at an alarming rate and has become a major public health concern worldwide. Recent epidemiological studies have provided direct evidence that DM is a strong risk factor for AD; this finding is now attracting attention. However, the underlying mechanisms for this association remain largely unknown. Previous in vitro and in vivo studies reported that diabetic conditions could cause an increase in the beta-amyloid pept

Emerging evidence suggests that diabetes affects cognitive function and increases the incidence of dementia. However, the mechanisms by which diabetes modifies cognitive function still remains unclear. Morphologically, diabetes is associated with neuronal loss in the frontal and temporal lobes including the hippocampus, and aberrant functional connectivity of the posterior cingulate cortex and medial frontal/temporal gyrus. Clinically, diabetic patients show decreased executive function, informa

Diabetes mellitus (DM) is one of the major non-genetic risk factors for Alzheimer disease (AD). However, the mechanism by which DM increases the risk of AD has not been elucidated. Here, we summarize recent findings to address this question. Whereas neuropathological studies in humans suggest that DM does not increase Aβ accumulation in the brain (a major hallmark of AD), earlier works in animal models show that Aβ does accumulate. Therefore, alternate mechanisms might exist. Recent studies usin

It is well known that a specific set of genetic and non-genetic risk factors contributes to the onset of Alzheimer disease (AD). Non-genetic risk factors include diabetes, hypertension in mid-life, and probably dyslipidemia in mid-life. This review focuses on the vascular and metabolic components of non-genetic risk factors. The mechanisms whereby non-genetic risk factors modify cognitive dysfunction are divided into four components, short- and long-term effects of vascular and metabolic factors

The benefits of statins, commonly prescribed for hypercholesterolemia, in treating Alzheimer's disease (AD) have not yet been fully established. A recent randomized clinical trial did not show any therapeutic effects of two statins on cognitive function in AD. Interestingly, however, the results of the Rotterdam study, one of the largest prospective cohort studies, showed reduced risk of AD in statin users. Based on the current understanding of statin actions and AD pathogenesis, it is still wor

Currently, there are more than 30 million dementia patients worldwide (1). More than half of dementia is caused by Alzheimer disease (AD), which consists of both familial and sporadic forms. Familial AD is caused by mutations in the amyloid precursor protein (APP) (2) and presenilin genes (3). Both mutations cause overproduction of amyloid-β (Aβ), particularly its longer form, Aβ42, which is more prone to aggregate. It should be noted that familial AD accounts for a small proportion of all AD ca