PubMed · 14092549
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Y GOTO. 1963. [CYTOCHROME C].. https://pubmed.ncbi.nlm.nih.gov/14092549/
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The present review shows that vascular parkinsonian syndrome (VPS) fulfilling stringent diagnostic criteria for parkinsonism is a rare disease that cannot always be distinguished from neurodegenerative parkinsonism on clinical grounds. Thus VPS needs to be differentiated from other disturbances, which have distinct phenomenological and therapeutical features including isolated gait disturbances associated with subcortical arteriosclerotic encephalopathy and neurodegenerative parkinsonism complicated by comorbid vascular encephalopathy. Acute or subacute VPS is usually caused by contralateral infarctions involving the external globus pallidus, ventrolateral thalamus, and, less often, the substantia nigra. Chronic VPS with insidious onset is related to bilateral subcortical infarctions affecting thalamocortical projections. Differentiation from degenerative parkinsonism is difficult in cases of VPS that display a progressive course and response to levodopa.
Matrix metalloproteinases are important factors for tissue remodelling and are activated during several physiological and pathological conditions, including cerebrovascular diseases. We give an overview of the structure, production and physiological effects of these widely distributed proteases and describe the genetic background and regulation pathways. In particular, we discuss the role of matrix metalloproteinases in vascular remodelling concerning ischaemic stroke, brain haemorrhage, vascular dementia, carotid artery plaques and cerebral aneurysms.
Homocysteine (Hcy) is a thyol amino acid resulting from de-methylation of methionine, an essential amino acid derived from dietary proteins. It is metabolized through two pathways: re-methylation and transsulfuration, which use as cofactors folate, vitamin B6 and vitamin B12. Hyperhomocysteinemia has been identified as a risk factor for cerebrovascular disease, dementia, impaired cognitive function and depression. Several drugs may interfere with metabolic pathways of Hcy, leading to an alteration of plasma Hcy levels. Lipid-lowering agents, used to reduce the risk of cerebral venous thrombosis or occlusive vascular disease in patients with high levels of plasmatic lipids, can increase plasma Hcy levels. Hyperhomocysteinemia has been also documented in Parkinson disease patients treated with levodopa and in epileptic patients after chronic treatment with antiepileptic drugs. In contrast, vitamins supplementations may be warranted in patients treated with lipid-lowering agents, levodopa and antiepileptic drugs in order to maintain normal plasma Hcy values. In contrast, higher doses of vitamins can induce dysfunctions in central and peripheral nervous system; therefore excessive supplements should be avoided.