Mitochondrial Health:
Is this the key to your wellbeing and longevity?

Mindd Foundation

Mitochondria and Alzheimer's

Understanding the role and impact of Mitochondrial Health on overall human health has been in the focus of research in the last decade. There is a good understanding of mitochondria’s role as the central powerhouses of human cells, but what are mitochondria actually responsible for and how does their health impact overall wellbeing?

At the 2019 Mindd International Forum, there was a particular focus on Mitochondrial Health. The keynote speakers, Dr Nancy O’Hara, Dr Liz Mumper, Dr Robert Naviaux and De Leila Masson are highly knowledgeable in this area and they revealed clinical insights to improve the health of all patients at a cellular level.

What are Mitochondria and What Are They Responsible For?

Mitochondria are a compartment, called an organelle, found inside the cell. They are mostly responsible for processing food and combining it with the oxygen we breathe, to generate energy known as adenosine triphosphate (ATP). This energy is then used to facilitate all the biological processes required to sustain human life. This biochemical process is called cellular respiration.

According to the United Mitochondrial Disease Foundation, mitochondria are responsible for generating over 90% of the energy required by the human body to facilitate organ function. If there is an issue with the generation of energy from mitochondria, cell injury and even cell death may follow. The organs that require the largest amounts of energy to function such as the heart, brain, kidneys and liver are most affected.

How Does Mitochondrial Health Impact Human Health?

Without effective mitochondrial functioning, growth and development would be hindered. Every day bodily processes such as digestion, cognition and cardiovascular function would also be affected. All human biochemical reactions require energy to facilitate them and this energy is created in the mitochondria, making their role irreplaceable.

Defence against Free Radicals and Oxidative Damage

Mitochondria are also involved in preventing the creation of free radicals and reversing oxidative damage. As a result of oxidative stress, damage to mitochondria is linked to the pathogenesis of a variety of disorders such as:

  • Schizophrenia
  • Bipolar disease
  • Alzheimer’s disease
  • Epilepsy
  • Migraines
  • Stroke
  • Neuropathic pain
  • Parkinson’s disease
  • Heart disease
  • Chronic fatigue syndrome
  • Fibromyalgia and more

Mitochondria act as the mediators throughout the process of apoptosis (cell death), which is important in ensuring that dysfunctional cells that could potentially be problematic are no longer biologically active. Whilst all cells are exposed to some level of oxidative damage, it is particularly important that mitochondria are able to understand the messages being sent to the cell and are able to respond accordingly. If the mitochondria cannot initiate cell death where required, further problems and disease states may progress.

What Factors Contribute to Weakening Mitochondrial Health?

Significant oxidative damage that affects inner membrane permeability can damage the mitochondria. Oxidative stress can be caused by certain medications, smoking, alcohol, environmental toxins, pesticides and a diet high in high-fructose corn syrup, sugar and refined carbohydrates. Genetic predispositions to mitochondrial disorders also play a role in mitochondrial health.

Science has a good understanding of the role of mitochondria as the central powerhouses of human cells, but what role do the play in ageing? Is mitochondrial dysfunction a risk factor for neurodegenerative disorders and the overall health of the human brain?.

Is there a Link Between Mitochondrial Dysfunction and Neurological Disorders?

As previously mentioned mitochondria are mostly responsible for processing food, combining it with oxygen, to generate energy known as adenosine triphosphate (ATP).

Thus, mitochondria are vitally responsible for providing the body’s energy. Disturbances to the process of mitochondria-provided energy result in altered innate function and have been identified as a critical area in the pathogenesis of many human diseases.

Neurological conditions are not immune to this. As mitochondria are critical regulators of cell death, reduced mitochondrial health and function has a key role in neurodegeneration. Ageing is also a significant risk factor in neurodegenerative diseases, and mutations in mitochondrial DNA and oxidative stress contribute to ageing.

What Changes can Mitochondrial Dysfunction Induce in the Human Body?

Mitochondrial dysfunction is a wide-ranging term explaining many cellular reactions caused by disturbed energy output. Changes that can occur due to disturbed mitochondrial health include:

  • reduced energy production
  • increased production of reduced oxygen species and therefore free radicals
  • altered gene signalling and
  • less control over the quality of a cell

Neurons have a vital requirement for mitochondria to supply ATP and a higher demand for oxygen, which means they are more susceptible to damage if the mitochondria are not functioning optimally. If neurons have lower levels of antioxidant defences, they are exposed to an increased level of free radical damage.

Mitochondria and Depression

There is evidence to suggest mitochondrial dysfunction is associated with depression due to new insights that the pathophysiology of depression may be linked to neuroplasticity and cellular resistance.

Mitochondria’s part in ATP production and cell signalling mean they have a permanent role in membrane stability, reactive oxygen species balance and to execute the complex processes of neurotransmission. These are all things that are now identified as contributors to the pathogenesis of depression.

Enhancing mitochondrial function appears to be a reasonable strategy for the treatment of neuronal function and, therefore, the management of mood disorders. This treatment may target specific mechanisms of mitochondrial dysfunction such as energy metabolism, synaptic plasticity and the survival of neurons.

Mitochondrial Dysfunction and Parkinson’s Disease

Parkinson’s disease (PD) is a disorder also associated with intellectual disabilities such as cognitive impairment. Like depression, dysfunctional mitochondria have a significant role in the pathophysiology of PD due to mutations of the mitochondrial genes and oxidative stress.

Since normal functioning of the mitochondria is essential for the energy requirements and cognitive processes in the brain, the underlying factors that can aggravate the function of mitochondria can, therefore, influence neurodegenerative processes and PD. Preclinical studies in different animal models have proven the involvement of mitochondria in disease pathology and conclude that mitochondrial dysfunction is one of the underlying contributors to the cognitive impairment process in PD.

Is there a link between the health of Mitochondria and Alzheimer’s?

Decades of evidence indicates that those who suffer from Alzheimer’s Disease (AD) have differing mitochondria than those who do not.

The research shows not only structural differences but also functional disparities. The current point of focus is to assess whether and how mitochondria may drive and mediate a variety of pathologies related to Alzheimer’s Disease (AD), to determine whether such a focus would be a valid therapy to the disease.

What is Alzheimer’s Disease?

As the second most common cause of death in Australia after Heart Disease (the fifth most common in the world), there is an increasing need for awareness and education surrounding AD and preventative methods.

Alzheimer’s Disease is best described as a degenerative neurological disorder caused by damage to nerve cells resulting in changes to the brain and brain tissue. Abnormal deposits of proteins form amyloid plaques, and nerve fibres become tangled throughout the brain. As a result, healthy neurons stop functioning and this causes the cells to die. More neurons become damaged as the disease progresses and tissue located in the brain shrinks significantly.

What is the Link Between Mitochondria and Alzheimer’s Disease?

Altered mitochondrial function has surfaced as one of the most plausible hypotheses related to the aetiology and pathogenesis of AD since mitochondria are implicated in cell survival and cell death pathways. Biochemical, molecular, animal, clinical and epidemiological research supports the idea that mitochondrial damage and oxidative stress are involved in the pathogenesis of AD.

Mitochondria are crucial for the preservation of membrane integrity, neurotransmission and synaptic plasticity. Considering that neurons have complex activity requiring a constant supply of energy and oxygen to survive, it comes as no surprise that tissue involved in the process of producing that energy can alter the activity of neuronal cells.

Not only that, mitochondrial function declines during ageing and ageing is the most predominantly known risk factor for AD.

Protecting Mitochondrial Health – Initial Clinical Interventions that were explored in-depth at Mindd Forum 2019

  • Antioxidants such as alpha lipoic acid, N-Acetyl Cysteine and coQ10
  • Exercise that stimulates mitochondrial biogenesis
  • An antioxidant and nutrient-rich diet. Some great examples of antioxidant-rich foods are berries, cherries, turmeric, cacao, broccoli, carrots, tomatoes, dark leafy greens and many more.
  • Vitamin B2 to support the citric acid cycle and energy production
  • Omega 3 Essential Fatty Acids to improve the cell wall function of a neuron
  • Ensure proper sleep as broken sleep will increase oxidative damage and neuronal plaques


Stay tuned for access to the full Video on Demand presentations from the Mindd International Forum 2019 – Coming Soon!

Mindd Foundation