Antioxidant Foods And Dementia

Dementia is invading the world as a current health problem, hitting nearly a population of over 50 million persons globally. Additionally, this number is expected to triple over the next twenty to thirty years. Meanwhile, we are expected to be ready for such challenges through a better understanding and management that covers both diagnosis and treatment.1

What is dementia?

Dementia is primarily considered as a drop in the cognitive functions that include judgment, critical thinking, behavior, linguistic functions, execution and memory. This decline seems to be gradual over a variable period up to years, a breakthrough that gives hope for stopping its progression in case of failure of prevention. Dementia has been associated with psychiatric disorders such as depression while affecting behavior. Yet, not all the components of the cognitive functions are usually affected in all of the suffering patients.2

Antioxidant foods and their effects on dementia

Although dementia seems to be well-defined, its mechanism of development in the human body is still undergoing debate among different studies. Nevertheless, the most prevalent theory is that dementia is a result of the loss of structure and function of the nervous system through a process called “neurodegeneration”. 

This deterioration may involve both the cells as well as the blood flow in the brain, resulting from several nasty irritants. Among these is the inability of the brain to get rid of its wastes, which include the products of the respiratory process in the brain. These latter are known as reactive oxidative species, whose accumulation has been linked to severe damage of the human cells in different tissues as well as cancers.

It is surprisingly interesting that antioxidants can potentiate the removal of not only these oxidative species away from the body, but also the scrambled abnormal protein wastes.

In addition, they  prevent any harmful interaction of the toxic products with the body cells.3

Consequently, Vitamin A, C, and E have shown a better improvement of cognitive functions in individuals with either a high intake or prolonged usage for 3 years. This is due to the activation of these vitamins for scavenger proteins of the oxidative species. In addition, they interfere with the abnormal accumulation of dementia-related toxic products such as amyloid beta 42 in Alzheimer's disease.4 These vitamins are easily found in citrus fruits and carrots.

Omega-3 fatty acids have shown their antioxidant effects especially in protecting the brain nerve cells from demyelination - a process of losing their protective and conductive sheath and processes. Omega-3 is found in fish and olive oil and is an essential component of a healthy Mediterranean diet.

More on dementia: symptoms, causes and treatment

Symptoms of dementia

The diagnosis of dementia is mostly clinical rather than a suggestive laboratory one. 

Some of the symptoms of dementia are: behavioural and psychological symptoms of anxiety; depression; psychosis; hallucination; delusion and aggression.5

Language functions are affected under the term of aphasia, up to the loss of fluency or inability of vocal expression. Additionally, the discrimination of sounds may get impaired.6

Memory is impaired at different levels. These include episodic memory which is the ability to memorise one`s life history, as well as semantic memory which is skills knowledge. Short-term memory is affected in severe cases which reflects the loss of the ability to memorise limited items within a limited time.7

Executive functions are much more affected, including visual and positional orientation as well as critical thinking.8

Causes of dementia

Dementia, as a consequence of neurodegeneration, has been attributed to multiple theories.

Oxidative stress is one of these; however, other theories continue to arise. The most widely known theory is the toxic product accumulation which classifies dementia types as the following:

Alzheimer's disease: constitutes 55-75% of causes of dementia with two strongly potential theories, such as:9

  • It is believed to result from the accumulation of toxic waste products called amyloid beta 42, exceeding the useful forms of amyloid beta 40  
  • The development is the accumulation of abnormal forms of functioning proteins known as Tau, which have an essential function of joining structural proteins in the brain cells. This may result in disruption of the functional organisation of the brain tissue

Vascular dementia: is considered the second most common cause of dementia. It is obviously related to the neurodegeneration of neurons and their intervening conduction due to the disruption of their blood flow. This may occur through one of the following:

  • Atherosclerosis of big blood vessels with fat deposition in their walls, which makes them less elastic to relax
  • Single or multiple small infarcts within the brain regions
  • Diseases of small vessels of the brain

All of these result in the function and structure of the brain neurons being in a deteriorated state, with a decreased probability of flushing out the brain's toxic products from the neurons, leading to further causes of dementia such as Alzheimer's disease.10

Parkinson's disease: constitutes approximately 15% of  dementia causes. It causes  neurodegeneration that affects the dopamine neurons with the accumulation of developed toxic particles, known as  alpha-synuclein and  ubiquitin. These are formed of abnormal proteins called Lewy bodies that contribute to a similar cause of  dementia called Lewy-body dementia. It is worth noting that the accumulation of such particles could interfere with the cycle  of  formation and breakdown of dopamine, an essential chemical transmitter for controlling neuronal function and integrity within some motor centres of the brain.11

Genes have been associated with numerous cases of dementia, suggesting the role of family history in cognitive decline and related dementia types.  Aberrations of genes such as the Apolipoprotein E gene were correlated to controlling Alzheimer's disease, either positively by preventing neurodegeneration through its E2 type, or negatively by potentiating neuronal loss through its E4 type. This gene was also linked to controlling the lipoprotein precursor levels, correlating the neuronal degeneration to the lipid profile accumulation which affects the blood vessels  with a probable result of vascular dementia as well.12 Another gene called Parkin has been related to Parkinson's disease.

Treatment for dementia

The variety in the types as well as the absence of a definitive potential theory of mechanisms of dementia has made the treatment of dementia difficult. While many studies have taken place toward finding a definitive theory, the majority of them failed to prove efficacy in humans after their success in experimental animals. This highlights the different nature of neurodegeneration in animals from humans as well as the discrepancy in their response to treatments, which may include several reasons. Among these reasons are the gene-influencing factors and the overlap of diagnoses between different types of dementia. This makes the treatment of dementia a treatment for symptoms rather than for a disease pathology.

We have to demonstrate the rising hopes of defeating the main cause of dementia, Alzheimer's disease, after the discovery of a few medications that target amyloid accumulation in the brain. One of them is Lecanemab which could succeed in slowing the disease progression in Phase III of a clinical trial, superseding its peer Gantenerumab which failed to prove its efficacy in the same phase.13


To sum up, dementia is a disease whose management requires united supportive efforts, rather than pharmacological treatment, due to our early stage of understanding. Science will always be an ocean that we see only at the peak of its rage. However, deeper diving is needed to see the bottom of its icebergs.  Hard work is needed to raise our awareness of  dementia, considering the simplest available prevention such as antioxidants.  All of this would help to reduce the rise in the number of dementia patients, if not eradicate it at the moment.


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  9. James BD, Bennett DA. Causes and patterns of dementia: an update in the era of redefining alzheimer’s disease. Annu Rev Public Health. 2019 Apr 1;40:65–84.
  10. Kalaria RN. The pathology and pathophysiology of vascular dementia. Neuropharmacology. 2018 May 15;134(Pt B):226–39.
  11. Béné R, Antić S, Budisić M, Lisak M, Trkanjec Z, Demarin V, et al. Parkinson’s disease. Acta Clin Croat. 2009 Sep;48(3):377–80.
  12. Yamazaki Y, Zhao N, Caulfield TR, Liu CC, Bu G. Apolipoprotein E and Alzheimer disease: pathobiology and targeting strategies. Nat Rev Neurol. 2019 Sep;15(9):501–18.
  13. van Dyck CH, Swanson CJ, Aisen P, Bateman RJ, Chen C, Gee M, et al. Lecanemab in early alzheimer’s disease. N Engl J Med. 2022 Nov 29; 

Mohamed Abulfadl

Master of Medical Biochemistry and Molecular Biology- Faculty of Medicine, Aswan University, Egypt

Mohamed is a medical doctor with neurology and nephrology research interest. He has an experience
of working for three years as a dual specialist of diagnostic Medicine (both diagnostic imaging and
Laboratory medicine).
Additionally, he has an interest in supporting university students, either as a teaching assistant, mentor
or even invigilator since 2016.
He is currently on a PHD study on translational neuroscience in Bristol medical school in UK. presents all health information in line with our terms and conditions. It is essential to understand that the medical information available on our platform is not intended to substitute the relationship between a patient and their physician or doctor, as well as any medical guidance they offer. Always consult with a healthcare professional before making any decisions based on the information found on our website.
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