Markers of brain illness may be hidden in your olfactory ability: a Japanese perspective.

There is evidence that impaired human cognitive abilities are reflected by loss of olfactory abilities. Declining olfactory perception may be a biomarker for impairment of cognitive function and of impending neurogenerative disorders. As olfactory perception may differ between culture and ethnic group, we sought to confirm this relationship with Japanese participants. In this study, we examined possible relationships between age and olfactory abilities in healthy Japanese subjects (control subjects) over a wide range of ages and compared this relationship with that observed in three neurodegenerative disorders; patients with Parkinson's disease (PD), Type 1 myotonic dystrophy (DM1) and Alzheimer's disease (AD). In control subjects, both threshold and recognition abilities decreased with age. Ability to detect odors was generally intact in most control subjects, however, we found that the abilities of individuals in the three different patient populations to recognize odors were impaired relative to control subjects. All three types of patients exhibited decreased or impaired odor-recognition compared with age-matched controls. Previous studies showed the causes of olfactory impairments in PD and AD patients were attributable to pathological changes and MRI signal abnormalities in limbic areas, including the amygdala (AMG), entorhinal cortex (ENT), hippocampus (HI), and orbitofrontal cortex (OFC). Another study reported that DM1 patients have bilateral lesions in anterior temporal areas, including the subcortical white matter, AMG, ENT and insula. Our findings underscore the need to pay careful attention to significant decreases of odor identification abilities caused by diverse forms of abnormal brain function, especially in the AMG, ENT and HI.

Donepezil abolishes anticholinergic activity in a patient with amnesia.

We report the case of a 74-year-old woman who presented with amnesia and positive serum anticholinergic activity (SAA), which disappeared after treatment with the cholinesterase inhibitor donepezil for 1 year. Her only other regular medications were topical glaucoma preparations. We suggest that mental stress, mild cognitive impairment and Alzheimer's disease pathology combined to generate SAA in this patient. We also consider that SAA may have subsequently become negative because of upregulation of acetylcholine production by donepezil, and because the patient's other medications and physical condition (including glaucoma) remained unchanged during the 1-year period.