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The Australian Imaging, Biomarker & Lifestyle (AIBL) Study of Ageing assesses the biomarkers, genetic factors, cognitive characteristics, and health and lifestyle factors that determine the development of Alzheimer’s disease.

Using this data, AIBL researchers make world-class contributions to understanding the natural history of Alzheimer’s disease progression.

The AIBL study commenced in 2006 with an original cohort of 1112 individuals aged over 60. Since then, over 1250 new participants have joined the study, with new recruits continuing to enrich the database.

The AIBL study is the largest of its kind in Australia, collecting data across more than 8500 person-years.

Our cohort

The baseline inception cohort of 1112 individuals included:

211

individuals with Alzheimer’s disease as defined by NINCDS-ADRDA

(McKhann et al., 1982)

133

individuals with Mild Cognitive Impairment¹

(Petersen et al., 1999; Winblad et al., 2004)

768

healthy individuals without cognitive impairment²

¹ A clinical syndrome characterised by reduced cognitive performance (often involving memory), which represents a high-risk state for the development of frank Alzheimer’s disease.

²This group included volunteers with at least one copy of the ApoE ε4 allele, volunteers without a copy of the ApoE ε4 allele and 396 volunteers who expressed subjective concern about their memory function. Memory complaints were elicited by the response to the question: ‘Do you have difficulties with your memory?’.

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OUR CHALLENGE

Why is AIBL important?

Alzheimer’s disease is the leading cause of dementia, accounting for 50–70% of all cases. Dementia is the leading cause of death and disability in Australians aged over 65. Australia’s ageing population makes it one of the country’s fastest-growing health and aged care issues.

Stock photo of health visitor talking to a senior woman during home visit.

While Alzheimer’s disease is not curable, delaying its onset by five years could nearly halve the cost of dementia to our society (Access Economics, 2005). Early intervention may increase a person’s quality of life, reduce stress and delay admission to residential care.

AIBL discoveries have helped develop new drugs recently approved by the US FDA for slowing the worsening of Alzheimer’s disease. Our study revealed the potential for very early treatment before symptoms develop, leading to current drug trials that could slow or stop the onset of dementia at this very early stage. AIBL is leading the development of new brain scans and blood tests to diagnose Alzheimer’s disease that will soon be in clinical use. We lead research into lifestyle factors and genetics that may allow an individual to understand and modify their risk of developing Alzheimer’s disease.

Alzheimer’s disease in Australia

#3

Source of spending

By 2040, Alzheimer’s disease is predicted to become the third-greatest source of health and residential care spending².

1.13M

PEOPLE WITH AD

With Australia’s ageing population, the number of people suffering from dementia is expected to reach 1.13 million by 2050, with Alzheimer’s disease being the most common cause².

$83B

In Spending

By the 2060s, spending on dementia is set to outstrip that of any other health condition and is projected to be $83 billion*.

*based on 2006–2007 dollars

¹ Australian Bureau of Statistics (2020)

² Access Economics (2009)

OUR MISSION AND VISION

What will AIBL achieve?

AIBL is committed to accelerating global research into the early detection and cause of Alzheimer’s disease. Through robust research and partnerships, we aim to:

DIAGNOSTICS

Determine a set of diagnostic markers, biomarkers and psychometrics that can be used to objectively monitor disease progression

EARLY DETECTION

Facilitate the early detection of Alzheimer’s disease

DELAYED ONSET

Develop hypotheses about diet and lifestyle factors that might delay the onset of the disease, providing preventative guidelines

CLINICAL PREVENTION

Enable the design of studies that may lead to clinically proven preventative strategies for Alzheimer’s disease

OUR WORK

Where is our research focused?

The AIBL study comprises six research streams, which help increase our value, impact and productivity.

FLUID BIOMARKERS

Blood and cerebrospinal fluid sample testing to examine differences between individuals diagnosed with Alzheimer’s disease and those without the disease.

Lifestyle

Research that examines the role of physical activity, sleep and diet in maintaining a healthy brain.

Neuroimaging

Structural neuroimaging scans using Magnetic Resonance Imaging (MRI), and beta-amyloid and tau Positron Emission tomography (PET) Imaging, to promote a better understanding of Alzheimer’s disease and facilitate earlier, more accurate detection and development of early therapeutic interventions.

Clinical AND Cognitive

Comprehensive clinical and cognitive assessments, including a neuropsychological assessment, measuring vital signs, recording medical and medication history and questionnaires about daily functioning, mood and lifestyle factors.

GENETICS

Research to increase our understanding of the role that genetics and epigenetic factors play in determining an individual’s risk of developing Alzheimer’s disease, the age of onset of the disease and how the disease progresses after its onset. Further research focuses on understanding how an individual’s genetics can guide preventative strategies, such as lifestyle interventions.

DATA AND MACHINE LEARNING

Use the latest ML/AI techniques to trawl through large data sets, aligning fluid/imaging-based biomarkers with cognitive and pathology-based outcomes.

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OUR IMPACT

What have we achieved so far?

Since 2006, data from the AIBL study has significantly contributed to international efforts focused on Alzheimer’s disease detection and prevention.

Key highlights

Improved understanding of the natural history of AD (i.e., when and where it starts and how long it takes).
Determined the effect of genetics (ApoE and BDNF) on the onset and progression of AD.
Optimised clinical trial design.
Supported the development of key fluid and imaging biomarkers—CSF, blood and PET tests.
Leveraging other grants (including ADNeT, ADOPIC, JPND, NHMRC, MRFF etc) and significant commercial buy-in.

Early detection

Developed new diagnostic criteria (Australian Cognitive Norms) that support earlier and more accurate Alzheimer’s disease diagnosis.
In-vivo validated the close association between beta-amyloid (Aβ) protein and Alzheimer’s disease in humans.
Identified a biomarker panel to differentiate healthy people from those with cognitive decline.
Determined that a panel of plasma proteins (comprising p-tau181, Aβ42/Aβ40 ratio and GFAP) have higher accuracy than each marker alone in differentiating cognitively healthy individuals with high brain Aβ from cognitively healthy individuals with low brain Aβ.
Determined that, longitudinally, plasma Aβ42/Aβ40 ratio decreased and plasma p-tau181 and GFAP increased faster in individuals with mild cognitive impairment compared with cognitively healthy individuals.

Determined that low plasma Aβ42/Aβ40 ratio and high plasma p-tau181, GFAP and NFL are associated with increased Aβ-PET load and prospective cognitive decline.
Higher plasma p-tau217+ was found in individuals with high brain Aβ (comprising healthy controls and those with mild cognitive impairment or Alzheimer’s disease) compared with individuals with low brain Aβ (comprising healthy controls and those with mild cognitive impairment and other dementia).
Determined that people with Alzheimer’s disease are more likely to be anaemic or have lower blood haemoglobin levels that are unexplained by dietary deficiency.
Determined that people with Alzheimer’s disease have elevated plasma homocysteine levels and decreased red cell folate levels.

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Imaging technologies

Established the diagnostic potential of beta-amyloid (Aβ) PET for Alzheimer’s disease versus other causes of dementia.
Determined the relationship of the level of brain Aβ with brain atrophy and cognition and the risks and rates of cognitive and clinical decline in normal, older persons and persons with memory impairment.
Revealed the relationship between the onset of Aβ accumulation and tau build-up in the brain.
Revealed the time course of Aβ accumulation and the later seen regional tau accumulation, opening a window for therapy development to prevent developing symptoms of Alzheimer’s disease.
Showed the relationship between astrocyte activation and early amyloid accumulation.
Served as the ‘gold standard’ for accuracy in developing blood tests for Alzheimer’s disease.
Revealed relationships between genetics and lifestyle factors with amyloid and tau pathology.

Lifestyle and prevention

Identified that older adults who participate in higher levels of physical activity have enhanced cognitive performance and lower levels of beta-amyloid (Aβ) and tau, the brain proteins implicated in Alzheimer’s disease.
Identified that older adults undertaking higher levels of physical activity have larger brain volumes.
Found that greater adherence to a Mediterranean diet in older adulthood is associated with less cognitive decline and less accumulation of brain Aβ over time.
Found that adherence to a Western diet and increased carbohydrate intake is associated with increased cognitive decline over time.
Found that higher coffee consumption is associated with less cognitive decline and less accumulation of brain Aβ over time.
Identified that prolonged time taken to fall asleep is associated with greater brain Aβ.
Showed that lifestyle may play a role in mitigating an increased genetic risk of Alzheimer’s disease.

Genetics and epigenetics

Developed significant evidence to show that the genetic factors that underpin the risk of developing Alzheimer’s disease are different from those associated with clinical progression.
Contributed to a large multi-centre study that showed the genetic architecture underpinning Alzheimer’s disease is more oligogenic than polygenic (i.e. fewer genetic variants were responsible for risk than previously reported).
Developed novel weightings to apply to measures of cumulative genetic risk (i.e. polygenic risk scores) that provide improved performance for predicting rates of disease progression over traditional methods.
Contributed to a large multi-centre study identifying novel resilience scores for those at high– genetic risk of Alzheimer’s disease.
Using DNA methylation analyses, found that individuals with higher epigenetic age compared to actual age had smaller brain volumes.
Showed that an individual’s genetic background is an important determinant of the relationship between lifestyle factors and Alzheimer’s disease pathological features—both levels and their rate of change.

Intervention

Found that in healthy older adults, anticholinergic drugs have a modest effect on psychomotor speed and executive function but no effect on other areas of cognition.

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AIBL on the global stage

The AIBL study has been published extensively in internationally recognised journals. The study is supported by pharmaceutical companies, the US Alzheimer’s Association and various private US philanthropic groups. Our research team receives regular requests to collaborate with national and international academics seeking AIBL data and blood samples for their research.

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OUR PUBLICATIONS

About AIBL