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Primary familial brain calcification [1] (PFBC), also known as familial idiopathic basal ganglia calcification (FIBGC) and Fahr's disease, [1] is a rare, [2] genetically dominant or recessive, inherited neurological disorder characterized by abnormal deposits of calcium in areas of the brain that control movement.
Cerebroretinal microangiopathy with calcifications and cysts (CRMCC) is a rare genetic disorder, which affects multiple organs. [ 1 ] [ 2 ] Its hallmarks are widespread progressive calcifications , cysts and abnormalities of the white matter of the brain, usually occurring together with abnormalities of the blood vessels of the retina .
Calcification is the accumulation of calcium salts in a body tissue. It normally occurs in the formation of bone, but calcium can be deposited abnormally in soft tissue, [1] [2] causing it to harden. Calcifications may be classified on whether there is mineral balance or not, and the location of the calcification. [3]
Cerebral atherosclerosis is a type of atherosclerosis where build-up of plaque in the blood vessels of the brain occurs. Some of the main components of the plaques are connective tissue, extracellular matrix, including collagen, proteoglycans, fibronectin, and elastic fibers; crystalline cholesterol, cholesteryl esters, and phospholipids; cells such as monocyte derived macrophages, T ...
Scientists have found a way to help Alzheimer’s drugs seep inside the brain faster — by temporarily breaching its protective shield. “Our goal is to give patients a head start,” by ...
Brain healing is the process that occurs after the brain has been damaged. If an individual survives brain damage, the brain has a remarkable ability to adapt. When cells in the brain are damaged and die, for instance by stroke, there will be no repair or scar formation for those cells.
Dystrophic calcification can occur even if the amount of calcium in the blood is not elevated, in contrast to metastatic calcification, which is a consequence of a systemic mineral imbalance, including hypercalcemia and/or hyperphosphatemia, that leads to calcium deposition in healthy tissues. [2]
The ligands cross the blood–brain barrier and attach to aggregated Aβ, and their retention in the brain is assessed by positron emission tomography. In addition, the presence of plaques and tangles can be estimated by measuring the amounts of the Aβ and tau proteins in the cerebrospinal fluid. [42] [43]