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Aggregation of β-amyloid (Aβ) in the brain begins to occur years before the clinical onset of Alzheimer's disease (AD). Before Aβ aggregation, concentrations of extracellular soluble Aβ in the interstitial fluid (ISF) space of the brain, which are regulated by neuronal activity and the sleep-wake cycle, correlate with the amount of Aβ deposition in the brain seen later. The amount and quality of sleep decline with normal aging and to a greater extent in AD patients. How sleep quality as well as

Age-related aggregation of amyloid-β (Aβ) is an upstream pathological event in Alzheimer's disease (AD) pathogenesis, and it disrupts the sleep-wake cycle. The amount of sleep declines with aging and to a greater extent in AD. Poor sleep quality and insufficient amounts of sleep have been noted in humans with preclinical evidence of AD. However, how the amount and quality of sleep affects Aβ aggregation is not yet well understood. Orexins (hypocretins) initiate and maintain wakefulness, and loss

Vascular dementia (VaD) is a history-laden disease entity that dates back to the 19th century when arteriosclerotic brain atrophy due to hardening of the arteries was perceived as the major cause of senile dementia. Its existence had been overshadowed by the emergence of Alzheimer's disease (AD) in the past century and research on AD dominated the field of dementia. Interest in VaD has been revived in recent years as vascular lesions have been shown to make great contributions to the development

INTRODUCTION: Recent studies have shown that pathologically defined subtypes of Alzheimer's disease (AD) represent distinctive atrophy patterns and clinical characteristics. We investigated whether a cortical thickness-based clustering method can reflect such findings. METHODS: A total of 77 AD subjects from the Alzheimer's Disease Neuroimaging Initiative 2 data set who underwent 3-T magnetic resonance imaging, [(18)F]-fluorodeoxyglucose-positron emission tomography (PET), [(18)F]-Florbetapir PE

Pain and depression were major detrimental factors affecting the physical and mental aspects of the HrQOL respectively. Therefore, the treatment of pain and depression can be important to improve the HrQOL.

Cortical laminar necrosis (CLN) is radiologically characterized by hyperintense cortical lesions on unenhanced T1-weighted images. Hypoxia is the representative cause of CLN; however, the rapid correction of hyponatremia has also been suggested as another possible cause. We present a patient who developed CLN and a permanent neurologic sequel following the rapid correction of hyponatremia without hypoxic insult, and discuss the characteristics of CLN lesions in view of osmotic demyelination synd

BACKGROUND: The challenges of the COVID-19 pandemic extend to concerns about vaccine side effects, particularly potential links to neurodegenerative diseases such as Alzheimer's disease (AD). AIM: This study investigates the association between COVID-19 vaccination and the onset of AD and its prodromal state, mild cognitive impairment (MCI). DESIGN: A nationwide, retrospective cohort study leveraging data from the Korean National Health Insurance Service was conducted. METHODS: The study, conduc

A substantial amount of amyloid-beta (Aβ) accumulates in the occipital cortices; however, it draws less attention. We investigated the clinical implications of Aβ accumulation in the occipital lobes in the Alzheimer's disease (AD) continuum. [18F]-Florbetaben amyloid PET scans were performed in a total of 121 AD or amnestic mild cognitive impairment (aMCI) patients. Of the 121 patients, 74 Aβ positive patients were divided into occipital Aβ positive (OCC+) and occipital Aβ negative (OCC-) groups

OBJECTIVE: As the fiberoptic gastroscopy using midazolam is being in widespread use, the exact nature of midazolam on memory should be clarified. We intended to examine whether midazolam causes selective anterograde amnesia and what impact it has on other aspects of memory and general cognitive function. METHODS: We recruited healthy subjects undergoing fiberoptic gastroscopy under conscious sedation. At baseline, history taking for retrograde amnesia and the Korean version of the Montreal Cogni

Progressive nonfluent aphasia (PNFA) is one of the language variants of frontotemporal dementia.1 Previously, PNFA, corticobasal degeneration (CBD), and progressive supranuclear palsy (PSP) were regarded as separate disease entities because of their distinctive clinical features and different anatomic involvement: left perisylvian area in PNFA,2 basal ganglia and dorsal midbrain in PSP, and perirolandic area in CBD.3 However, recent studies show that the 3 disorders share tauopathy and clinical

of equal size. Visual acuity was 20/20 in each eye. Mild proptosis without ptosis was observed on the right. No limitation was found in 6 cardinal extraocular movements without diplopia in any direction. Neither papilledema nor raised intraocular pressure was found on ophthalmological examination. The remaining neurological examination was normal. Examination for HLA-B5 and -B51 was positive. Laboratory works including complete blood count, muscle enzymes, sedimentation rate, C-reactive protein,