No association between hearing loss and amyloid-beta accumulation in the brain

Progressive hearing loss is relatively common in older adults. Studies show that almost 80% of adults older than 65 years have some degree of hearing loss (HL) which is greater than a 20 dB hearing level, as defined by the WHO criteria. HL limits social engagement, lowers quality of life, and amplifies the effects of cognitive impairment.  Previous studies have found an association between untreated hearing loss, Alzheimer’s disease and other types of dementia. People with hearing loss are therefore more likely to develop cognitive problems than people who do not have hearing loss. Indeed, some studies show that even mild HL is associated with almost twice the incidence of dementia and severe HL with a five-fold increased risk.

Alzheimer’s (AD) is the leading type of dementia globally, accounting for 60-80% of all cases. Two key neuropathologic features found in the brains of patients with AD dementia are the presence of plaques composed of beta-amyloid (Abeta) peptides and intracellular neurofibrillary tangles containing hyperphosphorylated Tau (tubulin-associated unit) proteins. These 2 groups of molecules are the most established biomarkers of the disease used in clinical and research practice. Buildup of these proteins can now be measured using positron emission tomography (PET) images and in cerebrospinal fluid. The complex pathophysiological relations between hearing impairment and dementia are unknown, but one theory is that HL could be a result of neurodegenerative processes that also lead to dementia. This is an area of intense research with many unanswered questions. For example, we still don’t know yet if hearing loss causes dementia, or vice versa. Thus, Australian scientists, Julia Sarant, David Harris, Peter Busby, Christopher Fowler, Jurgen Fripp, Colin Masters, and Paul Maruff decided to investigate the association between the HL and AD and particularly whether HL is an early biomarker for AD risk. The authors used the data of older adults enrolled in the Australian Imaging Biomarkers and Lifestyle (AIBL) Study. Individuals older than 50 years with no signs of dementia were selected (n=143). The participants underwent a hearing test and positron emission tomography (PET) imaging. They had a hearing assessment within 5 years of the brain scans and a cognitive evaluation within 2 years of their PET scan.

When researchers analyzed the data of the group, after taking age into account (as both amyloid in the brain and hearing loss increase with age) they found no association between the cognitive score, hearing loss, and amyloid-beta protein load. However, they found a positive association between the amyloid-beta protein load and positive Apolipoprotein E4 (APOE4) carrier status. The study, with the largest sample to date of preclinical older adults with HL, concluded that there is no association between positive amyloid-beta status and hearing loss. Hence, HL could not be regarded as a reliable early indicator of AD.

Researchers believe there is a need for more studies to understand the association of HL with AD. Associate Professor Julia Sarant from the University of Melbourne recommends future studies of the association between HL and neurodegenerative biomarkers of AD should be longitudinal, include larger samples, a greater number of people with hearing loss (with and without hearing aids), and objective assessments of hearing as well as central auditory processing (how the brain processes sound for speech understanding), in addition to assessment of cognitive abilities and brain neuroimaging.