Abstract
Alzheimer’s disease (AD), the most common cause of dementia in the elderly, is a neurodegenerative disorder associated with neurovascular dysfunction and cognitive decline. While the deposition of amyloid β peptide (Aβ) and the formation of neurofibrillary tangles (NFTs) are the pathological hallmarks of AD-affected brains, the majority of cases exhibits a combination of comorbidities that ultimately lead to multi-organ failure. Of particular interest, it can be demonstrated that Aβ pathology is present in the hearts of patients with AD, while the formation of NFT in the auditory system can be detected much earlier than the onset of symptoms. Progressive hearing impairment may beget social isolation and accelerate cognitive decline and increase the risk of developing dementia. The current review discusses the concept of a brain–ear–heart axis by which Aβ and NFT inhibition could be achieved through targeted supplementation of neurotrophic factors to the cochlea and the brain. Such amyloid inhibition might also indirectly affect amyloid accumulation in the heart, thus reducing the risk of developing AD-associated amyloid cardiomyopathy and cardiovascular disease.
Highlights
Alzheimer’s—A Systemic Disease?Alzheimers disease (AD) is a neurodegenerative disorder characterized by neurovascular dysfunction [1], cognitive decline [2], accumulation of amyloid β peptide (Aβ) in the brain [3] and the formation of tau-related lesions in neurons called neurofibrillary tangles (NFTs) [4]
We present a second hypothesis: the age-related imbalance of neurotrophic factors may be a link between AD and age-related hearing loss (ARHL)—-not in the sense of AD being affected by ARHL, but as a fundamental pathology such as neurovascular dysfunction
The aforementioned sections highlight the central role that investigations into neurovascular dysfunction in AD and ARHL have taken and highlight a number of interrelated mechanisms that may contribute to AD, AD-related amyloid cardiomyopathy and ARHL
Summary
Alzheimers disease (AD) is a neurodegenerative disorder characterized by neurovascular dysfunction [1], cognitive decline [2], accumulation of amyloid β peptide (Aβ) in the brain [3] and the formation of tau-related lesions in neurons called neurofibrillary tangles (NFTs) [4]. Aβ plaques are causally involved in cognitive decline [7,8], and elevated levels of Aβ in brain parenchyma may induce or promote neurovascular [9,10] and neuronal dysfunction [11]. This can lead to a cycle of self-propagation [12,13,14], as in a prion disease [15] and to cerebral β-amyloidosis [16]. We discuss innovative pursuits to inhibit the Aβ aggregation process and deposition in brain and heart more efficiently through targeted neurotrophic factor supplementation to the cochlea to prevent AD and the development of AD-related amyloid cardiomyopathy
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