Alzheimer’s disease (AD) is a terminal age-related disease that results in the loss of neurons from widespread parts of the brain.
AD affects over 20 million people worldwide and it is the leading cause of dementia. Little is understood about the causes of AD; in some cases genetic inheritance plays a role but the vast majority of AD patients develop the disease sporadically.
The brains of patients with AD tend to exhibit certain hallmarks of the disease including plaques made of a protein called beta-amyloid and tangles within the neurons of the brain that are associated with another protein called tau. Changes in tau are seen in a variety of other neurodegenerative diseases as well. However, while the development of these plaques and tangles has been implicated in the pathology of AD, it is uncertain whether they are a cause or an effect.
Currently, there are no approved treatments to halt or slow the progression of AD, though medications are available to treat the cognitive symptoms of the disease and potential new agents are currently under clinical trial.
Research in the Brain Repair Centre focuses on both the molecular and genetic causes of AD.
A variety of novel mutations in the tau gene are being created in BRC laboratories in order to study how the development of tau-related tangles in the brain contribute to neurodegeneration. For example, BRC researchers have demonstrated that pathogenic forms of tau disrupt the transport of important molecules within neurons, leading to their death.
Genetic studies of patients with AD have suggested particular genes that might increase a person’s susceptibility to the disease.
BRC investigators also have been at the forefront of demonstrating abnormalities in the tau protein in other diseases including Parkinson’s disease and frontotemporal dementia. F
inally, exciting new treatment possibilities also are being investigated, including a compound called scyllo-inositol which might prevent the development of protein aggregates in the brain and slow the progression of AD.
