There’s an unmet need to identify early pathophysiological biomarkers of dementia.
Loss of taste is complex and could serve to predict neurodegenerative disease.
Gustatory assessment in the clinic may include either electrical testing via a weak anodal current or psychophysical tests utilizing chemical stimuli to measure the ability to perceive the basic taste qualities.
Neurodegenerative diseases, such as Alzheimer’s disease and Parkinson’s disease, are often diagnosed post-mortem. The identification of neuropathological changes that present decades before severe clinical features could be helpful when applying disease-modifying treatments.
In the case of dementia, one such change could be gustatory loss.
Mechanisms of taste
Gustatory anatomy is complex and involves chemosensory perception at the level of the mucosal surfaces of the oral cavity, pharynx, larynx, and upper esophagus. The authors of a meta-analysis published in Neuropsychology Review explain the process of taste perception.
In basic terms, cranial nerves transmit information from taste receptor cells to the gustatory nucleus in the medulla oblongata, to the thalamus, and then to the primary gustatory cortex. Subcortical areas are also involved in gustatory processing, including the lateral hypothalamus, which moderates satiety. The hedonic importance of taste plays a major role in its psychological impact and likely involves the amygdala, thus being emotionally regulated.
Nevertheless, tastes are not simply “hedonic alterations of the Epicurean canon of gastronomy,” according to the authors of a chapter on taste disorders in disease. They note that “taste disorders can worsen and even compromise vital functions (malnutrition and aggravation of an underlying disease) and they always reduce quality of life.”
In neurocognitive disorders, write the Neuropsychology Review authors, both central mechanisms (relating to taste-information processing) and peripheral mechanisms (involving transmission of sensory receptors) have been implicated in observed gustatory impairment.
Even though the regions in the brain involved with taste and cognition overlap, there is less information on gustatory function in such disorders than on smell—most likely because tests for gustatory function are uncommon in the clinic. Also, the bilateral existence of the three cranial nerves involved in taste (glossopharyngeal, vagus, and facial) may help explain the resilience of taste to injury.
Japanese investigators conducted a small study evaluating gustatory function in patients with semantic dementia (SD) or Alzheimer's disease (AD) vs controls. They assessed the detection and recognition thresholds of four basic tastes: sweet, salty, sour, and bitter. The results indicated that the total detection and recognition threshold values were significantly higher in the SD and AD arms compared with the control group.
Patients with early stage SD demonstrated significantly higher detection and recognition thresholds vs controls, whereas increases in recognition threshold were observed only in AD patients. Patients with SD had higher thresholds for the detection of sweet and salty tastes, as well as the recognition of salty, sour, and bitter tastes compared with the control group.
On the other hand, AD patients demonstrated higher thresholds for only the recognition of salty and sour tastes.
“Taste discrimination was preserved, whereas taste identification was disturbed, in both the SD and AD groups,” the authors wrote. “Patients with SD performed significantly worse than both controls and patients with AD on the taste-to-picture-matching task, suggesting that semantic memory for taste may be impaired in ways similar to those observed for other modalities of semantic memory. Researchers have reported that the temporal poles may be associated with deficits in flavor identification.”
Other research has shown that alteration in the cortical processing of sensory taste occurs during the prodromal stage of AD and in individuals with mild dementia. It is not, however, present in patients with mild cognitive impairment.
Compromised gustatory function is also related to Parkinson’s disease, vascular dementia, alcohol use disorder, and frontotemporal dementia.
Potential clinical implications
Gustatory assessment in the clinic may include either electrical testing via a weak anodal current or psychophysical tests utilizing chemical stimuli to measure the ability to perceive the basic taste qualities. Electrical testing is popular in Japan. Such gustatory tests can be further parsed into whole-mouth and regional tests.
The Neuropsychology Review authors state that, before taste testing can be used as a biomarker of neurocognitive disease, evidence of a causal relationship must be elucidated, which requires further research.
Questions that specifically need to be answered to establish an ontic relationship include the following:
Whether patients with neurocognitive diseases have poorer gustatory function than cognitively intact controls
Whether the severity of the neurocognitive disease is associated with changes to taste
Whether different features of taste sensitivity (ie, threshold, identification, intensity) could be differentially involved in neurocognitive diseases
Whether neurocognitive diseases due to different etiologies are associated with specific patterns of gustatory dysfunction (eg, overall impairment, dysfunction of specific taste qualities perception)
What this means for you
The use of taste testing to predict dementia and other neurodegenerative diseases is not yet evidence-based, although there is potential for such application. Research points to loss of taste potentially being related to various neurocognitive diseases. So, if a patient complains of gustatory compromise, it could hint at future neurological disease.