The anterior insula and rolandic operculum are key regions for flavour perception in the human brain; however, it is unclear how taste and congruent retronasal smell are perceived as flavours. The multisensory integration required for sour flavour perception has rarely been studied; therefore, we investigated the brain responses to taste and smell in the sour flavour-processing network in 35 young healthy adults. We aimed to characterise the brain response to three stimulations applied in the oral cavity—sour taste, retronasal smell of mango, and combined flavour of both—using functional magnetic resonance imaging. Effective connectivity of the flavour-processing network and modulatory effect from taste and smell were analysed. Flavour stimulation activated middle insula and olfactory tubercle (primary taste and olfactory cortices, respectively); anterior insula and rolandic operculum, which are associated with multisensory integration; and ventrolateral prefrontal cortex, a secondary cortex for flavour perception. Dynamic causal modelling demonstrated that neural taste and smell signals were integrated at anterior insula and rolandic operculum. These findings elucidated how neural signals triggered by sour taste and smell presented in liquid form interact in the brain, which may underpin the neurobiology of food appreciation. Our study thus demonstrated the integration and synergy of taste and smell.

In super-aged societies, high salt intake substantially increases the risk of stroke and cardiovascular disease. Perceived low salty taste often prompts the addition of table salt to food. However, it remains unclear how older adults perceive the nature and intensity of salty taste in the mouth and brain. We compared the perceptions of salty taste intensities of older adults with those of young adults. Participants were 74 healthy adults: 31 older (age, 60–81 years [65.0 ± 5.5 SD]) and 43 young (age, 21–39 years [25.0 ± 3.6 SD]). Our research project comprises three sequential experiments. This article reports on the first two, which were (1) static and (2) dynamic sensory evaluations of taste perceptions in the mouth. Participants assessed the taste of 0.3 M and 0.5 M sodium chloride solutions in two types of sensory evaluations: (1) a cup tasting test, in which they sipped the solution from cups, spat it out, and rated static salty taste intensity, and (2) a time-intensity sensory evaluation, in which the solutions were delivered to participants’ tongues through a custom-made delivery system while they recorded dynamic taste intensities on a hand-held meter. Older adults perceived significantly lower taste intensities than young adults (p = 0.004 and p < 0.001 for 0.3 M and 0.5 M, respectively). Reaction timings for both solutions did not differ, but the slopes for both concentrations were significantly lower for older adults than for young adults (p < 0.001). Using a standardized system allowed us to evaluate and directly compare real-time feedback on taste intensities according to age. This study is the first to characterize the time-intensity profiles of salty taste intensity in older adults. Our findings show that older adults do not take longer to recognize a salty taste, but their perception of taste intensity slowly increases, and yet remains lower than that of young adults. This suggests that older adults should be aware of the tendency to add more salt to their food to compensate for their low perceptions of salty taste. We would like to suggest them to savor and chew sufficiently during eating to optimize the perceived salty taste. Furthermore, our results offer a reference for ordinary citizens’ taste-intensity perceptions; our standardized system could be usefully integrated into clinical follow-up examinations and treatments.

Glutathione, a natural substance, acts on calcium receptors on the tongue and is known to enhance basic taste sensations. However, the effects of glutathione on brain activity associated with taste sensation on the tongue have not been determined under standardized taste delivery conditions. In this study, we investigated the sensory effect of glutathione on taste with no effect of the smell when glutathione added to a combined umami and salty taste stimulus. Twenty-six volunteers (12 women and 14 men; age 19–27 years) performed a sensory evaluation of taste of a solution of monosodium L -glutamate and sodium chloride, with and without glutathione. The addition of glutathione changed taste qualities and significantly increased taste intensity ratings under standardized taste delivery conditions ( P < 0.001). Functional magnetic resonance imaging showed that glutathione itself elicited significant activation in the left ventral insula. These results are the first to demonstrate the enhancing effect of glutathione as reflected by brain data while tasting an umami and salty mixture.

Background: Deterioration of the oral environment is one of the risk factors for dementia. A previous study of an Alzheimer’s disease (AD) model mouse suggests that tooth loss induces denervation of the mesencephalic trigeminal nucleus and neuroinflammation, possibly leading to accelerated tau dissemination from the nearby locus coeruleus (LC). Objective: To elucidate the relevance of oral conditions and amyloid-β (Aβ) and tau pathologies in human participants. Methods: We examined the number of remaining teeth and the biofilm–gingival interface index in 24 AD-spectrum patients and 19 age-matched healthy controls (HCs). They also underwent positron emission tomography (PET) imaging of Aβ and tau with specific radiotracers, ¹¹ C-PiB and ¹⁸ F-PM-PBB3, respectively. All AD-spectrum patients were Aβ-positive, and all HCs were Aβ-negative. We analyzed the correlation between the oral parameters and radiotracer retention. Results: No differences were found in oral conditions between the AD and HC groups. ¹¹ C-PiB retentions did not correlate with the oral indices in either group. In AD-spectrum patients, brain-wide, voxel-based image analysis highlighted several regions, including the LC and associated brainstem substructures, as areas where ¹⁸ F-PM-PBB3 retentions negatively correlated with the remaining teeth and revealed the correlation of tau deposits in the LC ( r = –0.479, p = 0.018) primarily with the hippocampal and neighboring areas. The tau deposition in none of the brain regions was associated with the periodontal status. Conclusions: Our findings with previous preclinical evidence imply that tooth loss may enhance AD tau pathogenesis, promoting tau spreading from LC to the hippocampal formation.