Trypsin inhibition: a potential cause of cobalamin deficiency common to the pathogenesis of Alzheimer-type dementia and AIDS dementia complex?
There is increasing evidence for an association between Alzheimer-type dementia (AD) and nutritionally independent cobalamin deficiency. Furthermore, low serum cobalamin values occur in a kindred with familial Alzheimer's disease (FAD) and histopathological confirmation of AD neuropathology. The Cobalamin deficiency could be either a consequence or cause of amyloidogenesis. Cobalamin deficiency is also associated with the acquired immunodeficiency syndrome (AIDS). A common pathogenic mechanism may exist for AIDS dementia complex (ADC) and AD, but there is no explanation at present for these associations. This paper presents the hypothesis that protease inhibition is a common factor in AD and ADC resulting in protein-bound cobalamin malabsorption and disrupted cobalamin metabolism.
Department of Clinical Neuroscience, Mölndal Hospital of Göteborg, Sweden.
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A
McCaddon
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B
Regland
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Fear
D015526:AIDS Dementia Complex / Q000209:etiology / Q000503:physiopathology*; D000544:Alzheimer Disease / Q000209:etiology / Q000503:physiopathology*; D006801:Humans; D008954:Models, Biological; D014357:Trypsin / Q000378:metabolism*; D014361:Trypsin Inhibitors; D014805:Vitamin B 12 / Q000378:metabolism; D014806:Vitamin B 12 Deficiency / Q000209:etiology / Q000503:physiopathology*
D014361:Trypsin Inhibitors; D014357:Trypsin; D014805:Vitamin B 12