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    Centenary Institute > Research > Alzheimer’s disease

Alzheimer’s disease

Alzheimer's disease is a progressive, degenerative neurological condition caused by nerve cell death resulting in shrinkage of the brain. We are looking at many aspects including diet and metabolism to solve this disease.

At Centenary our research into Alzheimer’s disease is looking at the cause and potential treatments around a number of areas. These include vascular ageing, nerve cell death and the role of our diet and metabolism.

Alzheimer’s disease is an age-related neurodegenerative disease that progressively affects memory and behaviour. Alzheimer’s disease is currently diagnosed by the presence of amyloid plaques and tau tangles. However, ongoing clinical trials with drugs directed to amyloid and tau have failed to demonstrate efficacy for Alzheimer’s disease.

Endothelial cells line blood vessels and are responsible for preserving the blood brain barrier. When endothelial cells age (or senescence) they become leaky and fail to inhibit inflammation.

The Vascular Biology Program have, for the first time, demonstrated senescent endothelial cells in the brains of mice and humans. These cells appear before plaques develop, at least in mice. We believe that vascular dysfunction, induced by the presence of these senescent cells, is a major underlying initiator of Alzheimer’s disease. Elimination of these cells or restoration of their normal function may be a new approach for treatment of Alzheimer’s disease.

Our work over the next years will be to prove that the senescent endothelial cells contribute to the initiation of Alzheimer’s disease. We will develop methods to eliminate the senescent cells or to restore their normal function and then determine whether this impacts on the rate or severity of the pathology of Alzheimer’s disease.

Professor Jennifer Gamble, Head of Vascular Biology Program received an NHMRC Ideas Grant to pursue this work over the next four years.

Dementia is now the second leading cause of death in Australia. In dementias such as Alzheimer’s disease and frontotemporal dementia, the cells of the brain degenerate, causing the characteristic loss of memory, language, concentration, and emotion.

Nerve cells (neurons) communicate via electrochemical signals, and the efficiency of this communication is dependent on a form of electrical insulation called myelin, a fatty substance that encases each neuron (like insulation on wires). The myelin-producing cells, called oligodendrocytes, also provide neurons with fuel for energy production and protect them from degeneration.

In research published in the prestigious Journal of Neuroscience, the Lipid Metabolism and Neurochemistry Laboratory team established a biochemical mechanism through which these oligodendrocytes and their myelin degenerate in Alzheimer’s disease. This is important, as understanding the disease process is the first step in creating treatments.

Our research establishes that therapeutics used to protect myelin in the de-myelinating disease multiple sclerosis could be repurposed to provide significant protection against loss of cognitive functions in dementia.

Associate Professor Anthony Don, Head of Lipid Metabolism and Neurochemistry Laboratory leads this research.

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  • Nearly 1 in 10 people over 65 in Australia have dementia. Alzheimer’s disease is the most common form of dementia, up to 70% of all people with dementia

  • Worldwide, around 50 million people have dementia, and there are nearly 10 million new cases every year

  • Dementia was the second leading cause of death in Australia in 2018

  • People with dementia account for 52% of all residents in residential aged care facilities in Australia

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Alzheimer’s disease is an age-related neurodegenerative disease that progressively affects memory and behaviour. Alzheimer’s disease is currently diagnosed by the presence of amyloid plaques and tau tangles. However, ongoing clinical trials with drugs directed to amyloid and tau have failed to demonstrate efficacy for Alzheimer’s disease.

Endothelial cells line blood vessels and are responsible for preserving the blood brain barrier. When endothelial cells age (or senescence) they become leaky and fail to inhibit inflammation.

The Vascular Biology Program have, for the first time, demonstrated senescent endothelial cells in the brains of mice and humans. These cells appear before plaques develop, at least in mice. We believe that vascular dysfunction, induced by the presence of these senescent cells, is a major underlying initiator of Alzheimer’s disease. Elimination of these cells or restoration of their normal function may be a new approach for treatment of Alzheimer’s disease.

Our work over the next years will be to prove that the senescent endothelial cells contribute to the initiation of Alzheimer’s disease. We will develop methods to eliminate the senescent cells or to restore their normal function and then determine whether this impacts on the rate or severity of the pathology of Alzheimer’s disease.

Professor Jennifer Gamble, Head of Vascular Biology Program received an NHMRC Ideas Grant to pursue this work over the next four years.

Dementia is now the second leading cause of death in Australia. In dementias such as Alzheimer’s disease and frontotemporal dementia, the cells of the brain degenerate, causing the characteristic loss of memory, language, concentration, and emotion.

Nerve cells (neurons) communicate via electrochemical signals, and the efficiency of this communication is dependent on a form of electrical insulation called myelin, a fatty substance that encases each neuron (like insulation on wires). The myelin-producing cells, called oligodendrocytes, also provide neurons with fuel for energy production and protect them from degeneration.

In research published in the prestigious Journal of Neuroscience, the Lipid Metabolism and Neurochemistry Laboratory team established a biochemical mechanism through which these oligodendrocytes and their myelin degenerate in Alzheimer’s disease. This is important, as understanding the disease process is the first step in creating treatments.

Our research establishes that therapeutics used to protect myelin in the de-myelinating disease multiple sclerosis could be repurposed to provide significant protection against loss of cognitive functions in dementia.

Associate Professor Anthony Don, Head of Lipid Metabolism and Neurochemistry Laboratory leads this research.

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