Ischemic changes in vascular dementia (VaD) are often associated with other dementias, such as Alzheimer's disease, and have been shown to accelerate the disease process. It is therefore important to control risk factors for cerebrovascular disease in all dementias. This review outlines the vascular lesions underlying VaD and describes practical treatments based on this condition.

The brain-heart axis denotes the intricate bidirectional communication vital for maintaining overall physiological balance, or homeostasis. Numerous studies underscore the profound impact of cardiovascular conditions on brain health. Conditions such as atrial fibrillation and left ventricular hypertrophy have been identified as potential contributors to cerebrovascular diseases and cognitive impairment. Utilizing of tools such as the electrocardiogram (ECG) are instrumental in identifying atrial fibrillation and left ventricular hypertrophy. Notably, findings from such diagnostic tests correlate with cortical microinfarcts and diminished cerebral blood flow. An elevated P-wave terminal force in lead V1 on an ECG has emerged as a promising indicator of left atrial abnormalities, serving as a potential precursor to atrial fibrillation and cognitive impairment. Ultrasound modalities, such as echocardiography and carotid ultrasound, offer additional insights into the intricate relationship between cardiac function and cognitive dysfunction. In addition to imaging techniques, blood-based markers of cardiac disease, including N-terminal pro-B-type natriuretic peptide (proBNP), high-sensitivity cardiac troponin T, and Growth Differentiation Factor 15, have been associated with cognitive impairment, emphasizing an intricate heart-brain connection. Although exploring the roles of these biomarkers holds significant promise for future research, the interconnectivity between cardiac biomarkers and the brain remains poorly elucidated. The numerous underlying mechanisms linking the heart and the brain continue to elude our understanding and warrant further investigation.

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a genetic small vessel disease leading to recurrent strokes and cognitive decline. Stroke prevention is essential in CADASIL patients, since recurrent strokes determine the prognosis. However, there is no proven treatment for stroke prevention in CADASIL, although antiplatelet therapy is commonly used. Previous studies indicated reduced cerebral blood flow and impaired vasoreactivity in CADASIL patients, contributing to disease progression. Lomerizine hydrochloride is a calcium channel blocker approved in Japan for migraine prophylaxis. It has been reported to selectively inhibit cerebral artery contraction, increase cerebral blood flow, and exhibit neuroprotective effects. Therefore, lomerizine is a potential therapeutic agent for CADASIL patients. Preliminary data suggest the efficacy of lomerizine for preventing recurrent strokes in such patients. The LOMCAD trial, a multicenter, prospective, single-arm clinical trial comparing historical controls, designed to evaluate the efficacy of lomerizine to prevent recurrent ischemic events in CADASIL patients with recent histories of cerebral ischemic events, is currently underway. The results of this ongoing study are anticipated.

Alzheimer’s disease (AD) is a common cause of dementia, characterized by progressive memory loss and various functional impairments in the brain. Amyloid β-proteins (Aβ) is a main component of senile plaques, which is a major pathological features of AD. According to the amyloid cascade hypothesis, the deposition of Aβ in the brain is a key stone of the pathogenesis of AD. During the past decade, several Aβ-targetted medications have been developed, and the clinical trials for AD have been performed so far. In this article, we summarize the clinical features of AD and the molecular mechanisms of Aβ. In addition, we focus a content about the transmissible potencies of Aβ pathology and the inactivation methods against Aβ aggregates to prevent the transmission of Aβ among individuals.

A 58-year-old woman presented to our hospital after she suddenly noticed symptoms of not being able to remember her smartphone password or safe deposit box number while she was at work. Magnetic resonance imaging (MRI) diffusion-weighted imaging (DWI) displayed hyperintensity in the right hippocampal CA1 region, and she was hospitalized with a diagnosis of transient global amnesia. Fifty hours after onset, MRI displayed hyperintensity in the bilateral hippocampal regions. In this patient, a lesion was detected early on MRI within 24 hours of symptom onset, and lesions were found bilaterally and symmetrically in the CA1 regions 50 hours after onset.