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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.
Dementia
Published in John W. Scadding, Nicholas A. Losseff, Clinical Neurology, 2011
More commonly, VCI results from diffuse small vessel disease causing widespread white matter change. This used to be called ‘Binswanger disease’. Patients present with gradual cognitive decline and no history of vascular episodes, and it may mimic AD. Clues include bradyphrenia and prominent frontal deficits with subcortical pattern of memory impairment. Neurological examination may reveal focal signs, such as hemiparesis, brisk facial and limb reflexes, vascular parkinsonism (gait apraxia) or pseudobulbar palsy.
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.