This paper aims to investigate the role and mechanism of autophagy in meningioma. A total of 182 meningiomas which diagnosed in the ultrastructural pathology department of Beijing Neurosurgical Institute, Beijing Tiantan Hospital from 1993 to 2021. Light microscope, electron microscope, western blotting and immunohistochemical staining were used. 182 meningiomas, 104 males and 78 females. There were 174 WHO grade 1 benign meningiomas, including 62 meningothelial types, 39 fibrous type, 58 transitional types, 15 angiomatous types, 6 WHO grade 2 cases, including 4 clear cell types and 2 atypical types, 2 WHO grade 3 anaplastic types. Transmission electron microscopy (TEM) showed that the incidence of autophagosomes as a high expression in 27 cases, most of which were meningothelial meningiomas. Immunohistochemical markers EMA, PR, Vimentin, SSTR-2, Ki67, and CD34 were positively expressed in most of the tumors, GFAP, S-100, desmin, C-erbB-2 expression were negative. Western blotting was used to detect the up-regulated proteins of LC3, Beclin1, and down-regulated proteins of Bax, Caspase3, mTOR, PI3K, Akt, S6 and 4EBP1in meningothelial meningiomas compared with the none –meningothelial control group.Autophagy is induced by down-regulating PI3K/Akt/mTOR signaling pathway molecules in meningothelial meningiomas, which can inhibit tumor apoptosis and promote tumorigenesis.

Thalamic infarction can result in a diverse array of symptoms, including motor and sensory deficits, memory and attention difficulties, and alterations in mood and behavior; these symptoms are collectively referred to as thalamic infarction syndrome. The neural mechanisms underlying these symptoms are not yet fully understood, hampering the development of effective and individualized treatments. The current understanding of the pathology of thalamic infarction syndrome is mainly based on conventional computed tomography/magnetic resonance imaging scans, which reveal blood supply to various nuclei groups and clinical features. Thalamic infarction syndrome can be categorized into four groups according to the affected territory and associated vascular syndrome. Recent advancements in neuroimaging techniques, which enable the precise identification of affected pivotal thalamic subnuclei, altered brain structures, white matter pathway integrity, abnormal neural activity, and maladaptive states of brain networks, can enhance our understanding of the clinical mechanisms and inform the development of more effective therapeutic strategies. This review summarizes research on the pathological neural mechanisms of thalamic infarction syndrome and highlights future directions.

Amyotrophic Lateral Sclerosis (ALS) is a progressive neurodegenerative disease for which there is currently no reliable treatment. Existing clinical diagnostic methods include neurophysiological examination, neuroimaging, and genetic testing, etc. In contrast, there is a relative insufficiency of data in neuropathology research, and the pathogenesis is still poorly understood. The neuropathological evaluation results obtained from autopsies of ALS patients and various organ and tissue samples are crucial resources for the study of this disease. The ALS Human Brain Bank is urgently needed for the basic and clinical research on this disease. However, currently there is no standardized protocol for such an ALS Brain Bank. Based on the "Standardized Operational Protocol for the Human Brain Banking in China", this Standardized Operational Protocol is drafted to provide a guideline for the construction and operation of ALS Brain Bank to ensure the quality and homogeneity in China and worldwide. This article focused on the collection of anti-mortem information, donation process, the harvesting, preservation and pathological evaluation of the brain, spinal cord, and other organ/tissue samples of ALS donors in the human brain bank. The establishment of ALS Brain Banks may foster the relevant research works and pave the way for the treatment of this disease.