Aluminum Neurotoxicity: From Subtle Molecular Lesions to Neurological Diseases


Series: Neurology – Laboratory and Clinical Research Developments
BISAC: MED056000

Aluminum is the third most abundant element in the Earth’s crust. In many of the previous experimental, epidemiological, pathohistological, biochemical and other research studies, aluminum, accumulated from the environment has been recognized as a very harmful substance to the human body. Aluminum intake usually happens unintentionally due to the fact that people know little about its prevalence in water, factory-processed foods, medicines, cosmetics, etc. When accumulated in human organs, it can cause severe damage, and even lead to chronic neurodegenerative diseases. Both oxidative and nitrosative stress can be the leading cause or contribute to its toxic effects in humans and animals. All of this is supported by the fact that mitochondrial dysfunction is the earliest stage of aluminum neurotoxicity. When oxidative damage occurs under the effects of free radicals, together with the decreased antioxidant protection — due to the decreased production of the chemical energy molecule (adenosine triphosphate) as well as reducing equivalents (both in and out of mitochondria) — then the conditions for the occurrence of a vicious circle in aluminum neurotoxicity are created. Aluminum also significantly interferes with the main steps of the synaptic neurotransmission, which may lead to the progression of neuropathies. The glutamate-glutamine pathway and numerous neurotransmitter transporters are affected as well.

Oxidative stress and the disruption of neurotransmission do not only exist when adult individuals are exposed to this neurotoxin, but also in individuals prenatally exposed to it as well, and these are expressed after birth. Numerous research studies, both in animals and humans, ex vivo and in vitro, quite clearly showed that aluminum can be associated with chronic neurodegenerative diseases. Additionally, there is a positive correlation between the exposure to aluminum and the pathophysiology of Alzheimer’s, Parkinson’s, Huntington’s disease, amyotrophic lateral sclerosis, and so on. One of the possible mechanisms for the generation/development of these diseases could be the disturbed homeostasis of essential metals and the appearance of unfolded or misfolded proteins that are mostly specific for a particular disease. In those research studies, the influence of aluminum on the generation of beta-amyloid, alpha synuclein, etc. was satisfactorily examined.

It is very difficult, however, to suppress aluminum neurotoxicity, as well as development and progression of the diseases caused by or associated with aluminum. This is the result of some complex mechanisms through which aluminum causes its deleterious effects, and which are also responsible for the existence of multiple targets for aluminum. It is, therefore, necessary to know how these mechanisms induce the damage, in order to be able to prevent or treat the damage once it occurs. A large number of substances, including active components in traditional medicine, medical drugs and substances which are used only experimentally, have been examined so far. The results of studies conducted so far are inconclusive and they require further research. According to all the aforementioned findings, it may be concluded that well-planned, prospective and randomized clinical trials are necessary in order to use any of these substances in humans.
(Imprint: Nova Biomedical)

Table of Contents

Table of Contents


Chapter 1. Mechanistic Aspects of Aluminium Neurotoxicity: Oxidative Stress and Mitochondrial Dysfunctions
Vijay Kumar and Kiran Dip Gill (Dept. of Biochemistry, Postgraduate Institute of Medical Education and Research, Chandigarh, India)

Chapter 2. Aluminium and Imbalance in Neurotransmitter Release
Paula P. Gonçalves, Robert Zorec, and Virgília S. Silva (CESAM & Departamento de Biologia, Universidade de Aveiro, Aveiro, Portugal, and others)

Chapter 3. The Risk of Aluminium Neurotoxicity for Young Animals and Humans due to Multiple Exposure Opportunities, Particularly Perinatal
Mohammad Ahmad, Gasem M. Abu-Taweel, Jamaan S. Ajarem (Department of Medical Surgical Nursing, College of Nursing, King Saud University, Riyadh, Saudi Arabia, and others)

Chapter 4. The Protective and Dose-Dependent Effects of L-Name in Aluminium-Induced Neurotoxicity
Ankica Jelenković, Marina D. Jovanović, Nataša Petronijević, Toplica Lepić (University of Belgrade, Institute for Biological Research “Siniša Stanković”, Belgrade, Republic of Serbia, and others)

Chapter 5. Assail of Aluminum in Reference to Neurological Disorders
Shaik Afsar Pasha, Ch. Sindhu, Prasunpriya Nayak (Departments of Physiology and Neurology, NRI Medical College & General Hospital, Chinakakani, Mangalagiri Mandal, Guntur District, Andhra Pradesh, India)

Chapter 6. Link between Aluminum Neurotoxicity and Neurodegenerative Disorders with a Focus on Beta-Amyloid
Masahiro Kawahara (Department of Bio-Analytical Chemistry, Faculty of Pharmacy, Musashino University, Shinmachi, Nishitokyo-shi, Tokyo, Japan)

Chapter 7. Possible Neuroprotective Mechanism of Antioxidants against Aluminium Induced Cognitive Dysfunction
Anil Kumar, Arti Singh and Samrita Dogra (Pharmacology Division, University Institute of Pharmaceutical Sciences, UGC Centre of Advanced Study, Panjab University, Chandigarh, India)


Additional Information

Audience: Scientists in different fields, health professionals, industry of pharmaceuticals, food, cosmetics, dishes and aluminium production and applications.


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