Zinc diet and Alzheimer's disease: a systematic review

Abstract

The current state of evidence does not allow conclusions to be drawn on whether supplementation of Zn is beneficial for the prevention or treatment of AD, although a subclinical deficiency appears common in the elderly and subjects with AD. Dietary studies with animals suggest that the impact of dietary Zn on cognitive performance depend on additional nutrients. Further studies are necessary to determine whether Zn deficiency is a risk factor for AD in general terms or under certain dietary circumstances only.

Biological consequences of zinc deficiency in the pathomechanisms of selected diseases

“…Additionally, the extracellular amyloid plaques in AD brains are willing zinc binders, further depleting available zinc for neurons [120, 121]. Alternatively, another mechanism involved in AD and zinc action can be zinc’s capacity to inhibit calcineurin [122]. It has been postulated that a causative factor for AD is increased neuronal calcineurin activity because it adversely affects many downstream biochemical functions.…”

Importance and management of micronutrient deficiencies in patients with Alzheimer’s disease

“…Although they did not find conclusive evidence that could guide dietary Zn modifications to reduce the risk of AD, Loef et al73 claim, in a systematic review, that reduced Zn concentrations in AD patients might be related to disease risk. They suggest that a greater emphasis should be placed on an adequate supply of Zn to the elderly, either through increased consumption of Zn-containing food sources such as seafood, meat, nuts, and whole grains, or through supplementation in situations where food intake is insufficient, which is widely observed among AD patients.…”

Towards Primary Prevention of Alzheimers Disease

“…Copper is another substance often contained in multi-substance formulae of food supplements which, in the light of our review (Loef and Walach 2012), might be damaging rather than helping in respect to AD. In the case of zinc, it might be speculated that a subclinical deficiency increases the risk for AD (Loef, von Stillfried et al 2012). With the exception of iron, the evidence remains inconclusive.…”