China
Africa
Explore chapters and articles related to this topic
Genetics
Published in Ibrahim Natalwala, Ammar Natalwala, E Glucksman, MCQs in Neurology and Neurosurgery for Medical Students, 2022
Ibrahim Natalwala, Ammar Natalwala, E Glucksman
Binswanger’s disease (answer D) is a small vessel vascular dementia that results in memory loss and decline in cognitive ability. White matter lesions are thought to occur due to atherosclerosis. It usually presents in older persons.
B
Published in Anton Sebastian, A Dictionary of the History of Medicine, 2018
Binswanger Disease A progressive subcortical encephalopathy leading to a classic picture of dementia, which occurs mostly in the fifth and sixth decades of life. Described by a professor of psychiatry at Jena, Otto Ludwig Binswanger (1852–1929) in 1894. See subcortical dementia.
Regularity changes of the retinal nerve fiber layer and macular ganglion cell complex in patients with the amnestic mild cognitive impairment
Published in International Journal of Neuroscience, 2018
Yue Wu, Xiao-Ni Wang, Ningli Wang, Ying Han, Daqing Ma, Yan Lu
Exclusion criteria were: (a) retinal detachment, retinal artery occlusion, optic neuropathy, ocular trauma or surgery, diabetes mellitus, hypertension, cerebral infarction and other diseases which may affect RNFL thickness; (b) personal or family history of psychiatric disorders, anxiety, depression, dementia associated with Lewy body formation, frontotemporal dementia, vascular dementia, Creutzfeldt–Jakob disease, Binswanger disease, Parkinson's disease, multiple sclerosis and others; (c) some other serious chronic diseases.
Clinical implications of extracellular vesicles in neurodegenerative diseases
Published in Expert Review of Molecular Diagnostics, 2019
Other potential exosomal proteins for neurodegenerative disease-related disorders diagnosis have also been investigated. Xavier et al. explored the role of brain-derived EVs of chronically cerebral-hypoperfused mice on the intercellular communication mechanisms of the brain compared to early AD pathogenesis [54]. Differential proteome analysis of EV proteins isolated from the circulating blood and brain tissues of hypoperfused mice, post-mortem brain tissues of patients with early AD, and subjects with mixed dementia were assessed by high-throughput LC-MS/MS. In the study, both circulating and brain-derived EVs from hypoperfused mice contained shared proteins that were involved in various pathologic neuronal functions that resemble the EVs isolated from brain tissues of subjects with AD and mixed dementias. This data supports the existing evidence that cerebral vascular dysfunction contributes to AD pathology [94–98]. Moreover, hypoxia-associated proteins (e.g. mediators of cellular adaptation to hypoxia and angiogenesis) were identified across all groups, confirming the previous large cohort study (n = 465) that linked hypoxia conditions in brains of aging subjects to AD and Binswanger disease pathology [99]. Intriguingly, many proteins related to hypoxia-related responses, including the protein EFEMP1, a downstream activator of hypoxia-inducible factors (HIFs), were exclusively identified in brain EVs from hypoperfused mice, subjects with early AD, and mixed dementias, but not in age-matched controls. Collectively, these findings strongly support the role of hypoxia as an important early event leading to alterated brain EVs in the neuropathology of AD. More importantly, this study indicates that brain EVs are a promising source of circulating markers, and for the first time, provided data to suggest that a set of hypoxia-related proteins contained within EVs may aid in early diagnosis of AD.
Brain microvascular pathology in Susac syndrome: an electron microscopic study of five cases
Published in Ultrastructural Pathology, 2019
Dimitri P. Agamanolis, Richard A. Prayson, Negar Asdaghi, Sakir H. Gultekin, Kim Bigley, Robert M. Rennebohm
The microvascular changes in SuS, particularly collagen deposition, have also some similarity to hypertensive microangiopathy, including subcortical arteriosclerotic encephalopathy (Binswanger’s disease-BD) and age-related microvascular degeneration in the periventricular white matter.25 Both these conditions cause leukoencephalopathy, and light microscopy in both shows “fibrohyalinosis”, i.e., thickening, fibrosis, hyalinization, and narrowing of small blood vessels. The EM findings in BD and hypertensive MVD have not been described in detail. Light microscopic and immunohistochemical studies26 in BD show an obliterative microangiopathy with marked deposition of normally occurring collagens, increased BM components, splitting of the elastica in larger vessels, loss of smooth muscle, and no endothelial abnormalities. EM in age-related microvascular degeneration reveals microvascular thickening due to collagen deposits affecting the BM.25 The vascular injury in hypertensive microvascular disease and BD is caused by mechanical injury to blood vessels due to increased pressure. It has been suggested that age-related microvascular degeneration represents an adjustment to decreased perfusion, based on the fact that similar changes occur in the white matter of rats subjected to chronic hypoperfusion.27 However, there is more to the vascular pathology of SuS than mere fibrohyalinosis. EC degeneration and necrosis, cellular debris, lymphocytes, and other mononuclear cells, and obliterated fibrotic capillaries indicate that the vascular bed in SuS is the target of a destructive process rather than of a passive adaptation to hypoperfusion. BM thickening and microvascular fibrosis can be induced by different processes and types of vascular injury. In SuS patients who are young and normotensive, vascular injury is caused by an inflammatory process. SuS should be added to the list of inflammatory/immunologically mediated SVDs.28