Alzheimer's disease (AD) is one of the most common neurodegenerative diseases. Its etiology and associated mechanisms are still unclear, which largely hinders the development of AD treatment strategies. Many studies have shown that dysregulation of energy metabolism in the brain of AD is closely related to disease development. Dysregulation of brain energy metabolism in AD brain is associated with reduced glucose uptake and utilization, altered insulin signaling pathways, and mitochondrial dysfunction. In this study, we summarized the relevant pathways and mechanisms regarding the dysregulation of energy metabolism in AD. In addition, we highlight the possible role of mitochondrial dysfunction as a central role in the AD process. A deeper understanding of the relationship between energy metabolism dysregulation and AD may provide new insights for understanding learning memory impairment in AD patients and in improving AD prevention and treatment.

Alzheimer’s disease (AD) is characterized by the pathological accumulation of amyloid plaques and hyperphosphorylated tau proteins, leading to disruptions in synaptic transmission and neural circuit alterations. Despite advancements in therapies to delay disease progression, there is a pressing need for simple, non-invasive, and accessible biomarkers to evaluate their effectiveness. Quantitative electroencephalography (qEEG), a computational method for quantifying brain electrical activity, is increasingly applied in AD research. We highlight the application of qEEG biomarkers, including power spectrum analysis (oscillatory activity within frequency bands), functional connectivity (coherent neural couplings) and effective connectivity (directional neural interactions), microstates (brief, stable states of the brain network), and non-linear analyses (e.g., entropy and EEG network analysis). These biomarkers can reflect real-time neural dynamics, making them ideal tools for diagnosis and monitoring the progression AD and mild cognitive impairment (MCI). It has been shown that decreased α power and increased θ power within the qEEG spectrum correlate with enhanced AD severity. Data from microstate analysis have demonstrated significant variations in temporal dynamics in patients with AD. Non-linear measures, such as entropy, have identified marked reductions in neural complexity in AD and MCI patients, indicating that they may serve as early diagnostic markers. Compared to traditional neuroimaging techniques, such as magnetic resonance imaging (MRI) or positron emission tomography (PET), qEEG is known to be cost-effective and facilitates real-time monitoring. Overall, qEEG biomarkers are promising for advancing AD research due to their non-invasive nature, affordability, and ability to capture real-time neural activity. Integrating qEEG with multimodal neuroimaging and clinical profiles may facilitate earlier identification and precision therapies. Future research should focus on standardizing protocols, validating biomarkers across diverse cohorts, and exploring their potential in large-scale clinical trials.

As an adverse immune phenomenon, graft-versus-host disease often occurs after allogeneic hematopoietic stem cell transplantation. The incidence of acute and chronic graft-versus-host disease is about 40–60% and the mortality rate can reach 15%, which is a potentially fatal disease. There are rare GvHD cases involving the central nervous system. We reported a rare case of diffuse white matter changes after haploid bone marrow transplantation, summarizing its clinical manifestations and diagnosis and treatment in conjunction with the literature.

Hashimoto's encephalopathy (HE), also known as steroid responsive encephalopathy associated with autoimmune thyroiditis (SREAT), has a variety of clinical manifestations, with various neuropsychiatric characteristics, including tremors, transient aphasia, seizures, altered consciousness, myoclonus, cognitive impairment, and psychiatric manifestations. The hallmark presenting feature is a non-specific encephalopathy characterized by alteration of mental status and consciousness ranging from confusion to coma and impaired cognitive function, while those with cerebellar ataxia as the main manifestation is rare. We reported a case of Hashimoto's encephalopathy with cerebellar ataxia as the main manifestation, elevated anti-thyroid antibodies (anti-TPO/TG), and normal thyroid function. The symptoms of cerebellar ataxia improved after steroid treatment. Meanwhile, we reviewed the clinical features of 20 representative cases of HE with cerebellar ataxia as the core symptoms. In conclusion, based on our case findings and literature review, the diagnosis of HE should be suspected in cases of encephalopathy without an obvious cause, to quickly start an effective treatment.