Alzheimer’s disease (AD) is a progressive neurological disorder primarily recognized for its impact on memory and cognitive function. While the public often associates the condition with difficulties in recalling recent events, the disease also causes a significant decline in sensory abilities. This neurodegeneration targets the brain’s ability to process external information, profoundly changing how a person interacts with their environment. Sensory decline often begins subtly, even before the more recognized cognitive symptoms become apparent.
The Earliest Indicator: Impairment of Smell
The sense of smell, or olfaction, is widely considered one of the first and most reliable sensory functions to show decline in Alzheimer’s disease. Olfactory dysfunction is present in about 85% to 90% of AD patients, often years before a formal diagnosis of cognitive impairment is made. This makes the ability to smell an important potential early biomarker for the disease. The impairment is usually a reduced ability to detect or correctly identify odors (hyposmia), rather than a complete loss of smell (anosmia).
This vulnerability is directly linked to AD pathology. Neurofibrillary tangles (Tau protein aggregates) are frequently found in the olfactory bulb and its projection areas early in the disease course. Olfactory pathways connect directly to memory regions, such as the entorhinal cortex and the hippocampus, which are among the first areas damaged in AD. A decline in odor identification performance is associated with a greater buildup of amyloid and tau proteins in these regions. A poor sense of smell can lead to safety concerns, as individuals may fail to detect dangerous odors like smoke or spoiled food, and it can also contribute to a reduced appetite.
Visual Processing Challenges
While standard visual acuity often remains intact, Alzheimer’s disease causes significant challenges in visual processing—how the brain interprets images received from the eyes. The problem lies not with the eye, but with damaged areas in the brain’s visual center, located in the occipital and parietal lobes. These deficits include difficulty judging distances, perceiving contrast, or recognizing motion.
Patients may struggle with tasks such as navigating stairs, pouring a drink, or finding a misplaced object because the brain misinterprets the visual field. This is known as visual agnosia, where the person sees the object but cannot recognize or interpret it correctly. For instance, a black rug on a light-colored floor might be misinterpreted as a dangerous hole, leading to confusion and hesitancy. A specific, rarer variant of Alzheimer’s, Posterior Cortical Atrophy (PCA), begins with severe visual and spatial problems, as the pathology concentrates in the posterior brain regions responsible for vision.
Impacts on Taste and Hearing
The senses of taste and hearing are also affected by Alzheimer’s disease, often through different mechanisms than those affecting smell and vision. Taste decline (gustatory dysfunction) is frequently an indirect consequence of the loss of smell. Since olfaction accounts for a large part of flavor perception, the inability to smell food correctly leads to a diminished sense of taste enjoyment.
This loss of flavor can contribute to altered eating habits, reduced appetite, and unintended weight loss. Changes in brain regions responsible for processing taste and food-related decisions further complicate the issue, sometimes leading to altered food preferences. Regarding hearing, the primary issue is often not peripheral hearing loss—the ear’s ability to detect sound—but rather a central auditory processing deficit. The brain struggles to process complex auditory information, making it difficult to distinguish speech from background noise or understand rapid conversation.
Neural Basis of Sensory Decline
The underlying reason for these sensory changes is the accumulation of misfolded proteins, amyloid-beta (Aβ) and Tau. These proteins form plaques and tangles that damage neurons and disrupt the neural circuits responsible for sensory input and integration. Pathology is often more pronounced in the sensory association areas and superficial cortical layers of the brain, explaining why higher-level processing functions are impaired while basic sensory detection remains relatively preserved.
Tau tangles are observed in the olfactory bulb and the temporal lobe, correlating with the early decline in smell and later difficulties in auditory processing. The parietal and temporal lobes, which integrate visual and spatial information, are vulnerable to damage from both amyloid and tau pathology, leading to visual processing deficits. The synergistic action of Aβ and Tau pathology impairs these neuronal circuits, resulting in the profound sensory deficits that manifest as the disease progresses.