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-infarct 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 bloodbrain barrier in SDAT and AD, not in MID. Discussed is the possibility that in a large sub-group 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 co-existent 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.
Source: PSYCHIATRY (CANADA), 1984, 13/2 (97-104)