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Alzheimers disease/alcohol dementia: association with zinc deficiency and cerebral vitamin B12 deficiency
| Content Provider | Semantic Scholar |
|---|---|
| Author | Tiggelen, C. J. M. Van |
| Copyright Year | 1984 |
| Abstract | It is demonstrated that patients with senile dementia Alzheimer's type (SDAT) and alcohol related brain damage (AD) show a significant increase in ratio se-Cu/se-Zn when compared with patients with multi-infract dementia (MID) and when compared with a matched control group. This is regarded as an indicator of zinc deficiency and relative copper toxicity in SDAT and AD, not in MID. In the same groups with SDAT and AD a high incidence of pathologically low levels of vitamin B12 in cerebrospinal fluid (CSF) was found, despite normal serum B12 levels. In MID the normal serum B12 corresponded with a normal CSF B12. This indicates abnormal function of the choroid plexus and possibly of the blood-brain barrier in SDAT and AD, not in MID. Discussed is the possibility that in a large subgroup of SDAT and AD the clinical, neurochemical and neuropathological data can be explained by the hypothesis that the combination of zinc deficiency and copper toxicity results in limbic disinhibition and defective central noradrenergic neurotransmission. The neuroendocrine effects of the limbic disinhibition and the impaired regulation of the cerebral micro-circulation by the defective noradrenergic system will result in dysfunction of the blood-brain barrier and the choroid plexus, resulting as has been demonstrated in a CSF B12 deficiency. Such an effect is strongly potentiated by a coexistent depression. Due to the reduced plasticity of the aging brain the presentation of this organic affective syndrome and/or depression is under a "dementia" disguise, facilitated by organic cerebral changes caused primarily by zinc deficiency and copper toxicity, secondarily by the cerebral B12 deficiency. Early recognition and adequate treatment with nutritional supplementation can possibly prevent irreversible damage in subgroups of SDAT and AD. Primary prevention by nutritional strategies can be a realistic perspective. The need for further research into this challenging hypothesis is stressed. 1. Boswijk, Dept. of Geriatric Psychiatry Psychiatric Hospital "Voorburg", Vught — 5260 GB The Netherlands. Present Address: Farmers Road, Meeniyan, 3956 Victoria, Australia. Presented at Victorian State Geriatric Conference, La Trobe University, Melbourne, Australia. 1983. |
| Starting Page | 97 |
| Ending Page | 104 |
| Page Count | 8 |
| File Format | PDF HTM / HTML |
| Volume Number | 13 |
| Alternate Webpage(s) | http://www.orthomolecular.org/library/jom/1984/pdf/1984-v13n02-p097.pdf |
| Language | English |
| Access Restriction | Open |
| Content Type | Text |
| Resource Type | Article |
