Homocysteine in Neurology: A Possible Contributing Factor to Small Vessel Disease

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Rita Moretti; Mauro Giuffré; Paola Caruso; Silvia Gazzin; Claudio Tiribelli


Scholarcy highlights

  • This article aims to define the role of Hcy in the development of small vessel disease and neurological damage
  • Homocysteine accumulation could interfere with endothelium dysregulation, favor oxidative damage, and promote neuroinflammation and neurodegenerative processes
  • A relatively recent study produced contradictory results in coronary stenosis, the prevalence of significant coronary artery stenosis, atherosclerotic, calcified, mixed, and non-calcified plaques increased with homocysteine
  • Homocysteine is not associated with an increased risk of subclinical coronary atherosclerosis
  • While many studies focused on thrombosis and HHcy, HHcy and coronary disease, stroke, and major vessel disease, few data are available on HHcy and vascular and neurodegeneration because SVD in the brain is a relatively recent entity
  • SVD is a complex clinical entity linked to the aging modification of the small arteries, altered endothelium activation, oxidative damage, and generally by a chronic inflammatory state induced by persistent hypoperfusion
  • Definition of the different roles of Hcy at the different cellular levels, promotion of the confluency of altered white matter areas, and times of the development of small vessel disease in the brain may provide hints as to the modulation of Hcy to prevent disease

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