Zinc and brain diseases

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1. Alzheimer's disease

Alzheimer's disease is the most common progressive dementia affecting the elderly today. It is a multifactorial disease of both genetic and non-hereditary causes. The basic theory of Alzheimer's pathogenesis focuses on the accumulation of amyloid-β (Aβ).
It was observed that zinc can precipitate Aβ, leading to the accumulation of plaques - the main pathological hallmark of Alzheimer's. In addition, there is more evidence for the involvement of zinc in Aβ deposition in Alzheimer's disease in mice.
Plaque quantity and size was also enhanced when dietary zinc was adjusted. These data may reflect the diverse roles of zinc in the regulation of Aβ and . Along with the effects of zinc, other metals (such as copper) have also been reported to be involved in the development and progression of Alzheimer's-like brain diseases, but these observations are uncertain and the Researchers are still continuing to evaluate what disease zinc deficiency causes.

2. Amyotrophic lateral sclerosis (ALS syndrome)

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease of the human motor system that can be fatal. Approximately 5-10% of cases run in families and 90% are sporadic. The most common cause of familial ALS is a genetic mutation related to copper and zinc. This mutation increases toxic function in motor neurons under prolonged zinc deficiency.
In addition, zinc in the spinal cord of patients with sporadic ALS was also down-regulated, suggesting that zinc also plays a role in pathogenesis. In another study, zinc levels in the cerebrospinal fluid of patients with ALS were also significantly higher. However, the exact mechanism underlying this increase and the potential effects still need to be elucidated.

3. Traumatic brain injury

A traumatic brain injury is a disruption of the normal structure and/or function of the brain, which may result from a blow or concussion to the head, or from penetrating trauma to the head. This accident can damage neurons through direct mechanical damage (such as membrane rupture and diffuse axis damage) and indirect (through ischemia). Ischemia associated with traumatic brain injury (and ischemic stroke) initiates glutamate release, leading to toxicity and cell death of postsynaptic neurons.
Evidence suggests that synaptic zinc release can also cause nerve cells to be injured and killed under excitatory conditions. The results of studies in both ischemic and status epilepticus (a secondary complication of traumatic brain injury) clearly demonstrate an association with zinc. In particular, synaptic release of zinc has been shown to contribute to neuronal damage, and occurs concomitantly with glutamate release following head trauma. However, the role of zinc in brain damage remains unclear. For example, when studying a rat brain model of traumatic brain injury, zinc chelation contributes to the regulation of neuroprotective genes and reduces cell death, thereby suggesting a toxic role for zinc in this type of injury. this.

4. Depression

Depression affects millions of people worldwide, and is associated with many neurodegenerative diseases. Evidence for a role for zinc in depression has attracted much scientific attention over the past decade. It was observed that depressed patients had lower serum zinc concentrations than mentally normal subjects. Zinc levels were also inversely correlated with the severity of depressive symptoms. Furthermore, other studies indicate that serum zinc levels can be normalized after successful treatment of depression.

5. Schizophrenia

Schizophrenia is a long-term mental disorder, characterized by inconsistencies between thoughts, feelings, and behaviors, leading to misperceptions, inappropriate, detached actions and moods reality into fantasy and fantasy. This is a condition with both neurodegenerative and neurodevelopmental pathology with potential causes of prolonged maternal zinc deficiency and genetic risk factors. In the rat experiment, maternal zinc deficiency resulted in prenatal zinc deficiency, which reduced brain mass of the pups.
For patients with schizophrenia, brain zinc levels have been shown to decrease by 30 - 50% in cases of early onset. While prenatal zinc deficiency may not be the sole cause of the disease, interactions with other risk genes and/or continued zinc deficiency after birth may be a contributing factor. Other findings also suggest that disruption of zinc cellular homeostasis may be part of the pathophysiology of schizophrenia.

6. Parkinson's disease

Parkinson's disease is a long-term degenerative disorder of the central nervous system that mainly affects the motor system. Symptoms develop slowly over time, the most obvious being tremors, muscle stiffness, slow movements, and difficulty walking. Both thinking and behavior problems can occur, and dementia can also present in a more advanced stage of the disease.
Observation of patients with Parkinson's disease for clinical zinc deficiency. Animal studies with Parkinson's disease demonstrate the effectiveness of zinc supplementation, resulting in beneficial effects. For example, in flies that exhibit Parkinson's symptoms in humans, zinc supplementation improved muscle abnormalities, motor impairments, and loss of flight ability, as well as a severe reduction in life expectancy. important. Taken together these data suggest that zinc homeostasis is altered in Parkinson's disease, and thus may contribute to the pathogenesis.
In summary, zinc is an indispensable micronutrient for humans, zinc deficiency is associated with many disorders. In the central nervous system, maintaining zinc homeostasis is critical for brain health, particularly with regard to cognition. Altered zinc homeostasis is considered to be a contributing factor to the pathogenesis of various brain diseases.
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References: pubmed.ncbi.nlm.nih.gov