Alzheimer’s disease (AD) is a progressive neurodegenerative disorder primarily recognized for causing memory loss and cognitive decline. The disease involves the gradual destruction of brain cells, leading to atrophy in regions responsible for thinking, memory, and language. While memory decline is the most prominent symptom, AD also disrupts how the brain processes information from the outside world. Examining how AD affects the non-cognitive senses illustrates the far-reaching nature of the underlying brain pathology.
Olfaction: The Earliest Indicator of Decline
Olfaction, the sense of smell, is frequently the earliest sensory system to show impairment in individuals with Alzheimer’s disease, often beginning years before recognizable memory loss symptoms appear. The dysfunction can manifest as hyposmia (reduced ability to smell) or, in more severe cases, anosmia (the complete loss of smell).
This sensory deficit is closely tied to the neuropathological changes of AD in specific brain structures. The olfactory bulb, which receives initial input from the nose, and the entorhinal cortex, a key region for processing smell and memory, are among the first areas to accumulate pathological proteins. The entorhinal cortex serves as a gateway to the hippocampus, a major memory center, and its early damage affects both memory function and olfactory processing.
The loss of olfactory function is strongly linked to the accumulation of harmful amyloid-beta and tau proteins. Individuals who experience a greater decline in their sense of smell over time also show higher levels of this Alzheimer’s-related pathology in associated brain regions. Simple, non-invasive smell identification tests are being investigated as a potential tool for identifying individuals at risk for AD and mild cognitive impairment. Higher scores on these tests are associated with a reduced risk of transitioning from normal cognition to mild cognitive impairment and eventually to dementia.
Visual Processing Challenges
While the physical ability of the eyes to see often remains intact in early AD, the disease significantly impairs the brain’s capacity for visual processing. This means visual acuity, or 20/20 vision, can be normal, but the interpretation of the visual scene is corrupted. This phenomenon is often linked to a condition known as Posterior Cortical Atrophy (PCA), which is a visual variant of Alzheimer’s disease. In over 80% of PCA cases, the underlying cause is the same pathological buildup that characterizes AD.
The damage primarily affects the posterior regions of the brain, including the parietal and occipital lobes, which are responsible for complex visual interpretation and spatial awareness. This damage leads to difficulties with depth perception, judging distances, and accurately reaching for objects. Patients may struggle with identifying moving objects or recognizing familiar faces, a condition known as agnosia.
These individuals often visit eye doctors, mistakenly believing their problems stem from the eyes themselves, only to learn their eyes are healthy. The core issue is that the shrinking brain tissue in the posterior cortex can no longer properly process the information sent from the healthy eyes. Other symptoms include sensitivity to bright light and difficulties with reading, as the brain struggles to track text on a page.
Neuropathological Basis of Sensory Loss
The sensory deficits in both olfaction and vision are rooted in the characteristic biological changes of Alzheimer’s disease. The primary pathological hallmarks are the accumulation of amyloid-beta (Aβ) plaques outside of neurons and the formation of neurofibrillary tangles composed of hyperphosphorylated tau protein inside them. These protein aggregates disrupt the normal communication between neurons and ultimately lead to brain cell death and tissue atrophy.
In the case of olfaction, the pathology begins in the allocortex, which includes the entorhinal cortex, and the olfactory bulb, regions that are structurally connected to the main memory centers. This early involvement of the olfactory system makes smell loss one of the earliest measurable symptoms.
For visual processing, the pathology spreads to the posterior cortical areas, including the occipital and parietal lobes. This targeted damage to the visual processing centers, rather than the primary visual cortex, explains why interpretation of sight is impaired while the eyes’ physical function is preserved. Tau pathology tends to be more concentrated in these posterior brain regions in individuals who present with visual symptoms, compared to those with a more typical memory-focused presentation of AD.