Alzheimer’s disease (AD) is a complex, heterogeneous age-related disorder and the most common form of dementia. It is characterised clinically by a decline in cognitive and functional ability and the development of behavioural and psychological symptoms. At a cellular level, it comprises degeneration of neurons and synapses, formation of amyloid plaques and intracellular neurofibrillary tangles.¹

Diagnosis of AD requires neuropsychological testing, limited laboratory tests and brain imaging. Since pathology generally precedes symptoms, AD is diagnosed after clinical onset of the disease, at which stage the patient is already suffering from cognitive defects such as mild cognitive impairment (MCI).² Moreover, the diagnostic accuracy of neurodegenerative disorders is low, ranging from 50 to 85%.³

Current therapeutic options for AD are symptomatic treatments thattarget dysfunctional neurotransmitters associated with the disorder. The only approved therapies are c olinesterase inhibitors and one N-methyl-D-aspartate receptor antagonist. Use of these agents is widespread and long-term;4 however, they confer only moderate clinical effects in patients with mildly to moderately severe symptoms and do not affect the fundamental pathology of AD.5 The majority of recent research has focused on therapeutic strategies that inhibit the production and aggregation of amyloid beta protein (Aβ) in plaques and increase its clearance from the brain. Such strategies are likely to be most effective at pre-clinical stages of the disease, before widespread synaptic and neuronal loss occurs.¹

To read full article please click here.