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Binswanger's disease, also known as subcortical leukoencephalopathy and subcortical arteriosclerotic encephalopathy, [1] is a form of small-vessel vascular dementia caused by damage to the white brain matter. [2] White matter atrophy can be caused by many circumstances including chronic hypertension as well as old age. [3] This disease is ...
The most severely affected tissues are the myelin in the central nervous system, the adrenal cortex, and the Leydig cells in the testes. The long chain fatty acid buildup causes damage to the myelin sheath of the neurons of the brain, resulting in seizures and hyperactivity. Other symptoms include problems in speaking, listening, and ...
A deficiency in GALC thus causes a buildup of these fatty acids, leading to an incursion by cells called "globoid macrophages" that destroy oligodendrocytes, thereby inhibiting any further myelin formation. [20] Given the presence of globoid macrophages clustered near white matter, Krabbe disease often is called globoid cell leukodystrophy.
Leukoencephalopathy (leukodystrophy-like diseases) is a term that describes all of the brain white matter diseases, whether their molecular cause is known or unknown. [1] It can refer specifically to any of these diseases: Progressive multifocal leukoencephalopathy; Toxic leukoencephalopathy
The gray matter remains normal in all characteristics while the white matter changes texture, becoming soft and gelatinous. Rarefaction of the white matter is seen through light microscopy and the small number of axons and U-fibers that were affected can also be seen. Numerous small cavities in the white matter are also apparent.
Frontotemporal dementia (FTD), also called frontotemporal degeneration disease [1] or frontotemporal neurocognitive disorder, [2] encompasses several types of dementia involving the progressive degeneration of the brain's frontal and temporal lobes. [3] Men and women appear to be equally affected. [1]
The damaged white matter is known as "Normal-appearing white matter" (NAWM) and is where lesions appear. [10] These lesions form in NAWM before blood–brain barrier breakdown. [64] BBB can be broken centripetally (the most normal) or centrifugally. [65] Several possible biochemical disrupters were proposed.
Alexander disease causes the gradual loss of bodily functions and the ability to talk. It also causes an overload of long-chain fatty acids in the brain, which destroy the myelin sheath. The cause of Alexander disease is a mutation in the gene encoding GFAP. [2] [7] [4] [5] [11] [10] [excessive citations] A CT scan shows: Decreased density of ...