Abstract:
Alzheimer’s disease (AD) is hugely prevalent in the ageing population. It is estimated by 2050, more than 100 million people will be affected worldwide (Lin, 2013). The hallmark clinical features of this disease include a decline in cognition and memory. Characteristic histopathological hallmarks include the deposition of Beta- amyloid (Aβ) peptide and formation of intracellular neurofibirillary tangles (NFT) of hyperphosphorylated tau. Although the disease is well characterised, there has been little success on a cure or prevention for this debilitating disease. More recent advances suggest sensory deficits may be a risk factor in cognitive decline. Specifically, hearing loss has been associated with high transference rates from mild cognitive impairment to AD compared to hearing controls (Gates, 2011). Hearing loss is thought to play a role in the development of AD through a reduction in stimulatory input and hampering social interaction (Lin, 2011). It is thought that auditory dysfunction leads to an increase in cognitive load as a result of compensatory recruitment of other regions of the brain. It is hypothesised that the depletion of cognitive reserve leads to earlier expression of dementia symptomatology. Although it is very difficult to ascertain the relationship between hearing loss and the development of AD, if a relationship was established it may provide insight regarding the significance of restoring or maintaining auditory function on delaying AD dementia. In order to assess the relationship between AD and hearing loss it is first important to look at the anatomical changes that occur in the auditory pathway. Although this will not provide information on the direct relationship, it lays the foundation for further research to assess the role that both peripheral and central auditory dysfunction may play in AD. This study used histochemical and free-floating immunohistochemical (IHC) techniques to investigate changes in cytoarchitectural and neurochemical environment in the auditory cortex (AC) of 5 AD brains when compared with 5 age-matched normal brains. The findings from this study illustrate substantial changes in cytoarchitecture of the AC of AD patients demonstrated by cresyl violet staining and IHC staining for neuronal marker, NeuN and microtubule marker, SMI-32. Further, the AC or AD patients was affected markedly by the hallmark neuropathology of AD whereby Tau tangles and Aβ aggregates were found consistently throughout sections. Changes in cell morphology were illustrated in AD sections through staining for the calcium binding protein, parvalbumin, as well as changes in immune cells shown by antibodies directed against IBA1 (microglia) and GFAP (astrocytes).