Janice Knebl

<h3>Abstract</h3> <h3>Background:</h3> We evaluated smell identification as a biomarker for Alzheimer disease (AD) by assessing its utility in differentiating normal aging from an amnestic disorder and determining its predictive value for conversion from amnestic mild cognitive impairment (aMCI) to AD. <h3>Methods:</h3> Cross-sectional study (AD = 262, aMCI = 110, controls = 194) measuring smell identification (University of Pennsylvania Smell Identification Test [UPSIT]) and cognitive status was performed, as well as longitudinal analysis of aMCI participants (n = 96) with at least 1 year follow-up (mean 477.6 ± 223.3 days), to determine conversion by National Institute of Neurological and Communicative Disorders and Stroke–Alzheimer’s Disease and Related Disorders Association criteria. <h3>Results:</h3> Odor identification and disease status were highly correlated after correcting for age, sex, and <i>APOE</i> (<i>p</i> &lt; 0.001). Receiver operating characteristic (ROC)/area under the curve (AUC) was similar for the 40-item UPSIT, the top 10 smells in our study, and the 10-item subset previously proposed. Smeller/nonsmeller based on the 10-item subset with a cutoff of 7 (≤7, nonsmeller; &gt;7, smeller) had a sensitivity and specificity of 88% and 71% for identifying AD and 74% sensitivity and 71% specificity for identifying an amnestic disorder. A total of 36.4% of participants with impaired olfaction and 17.3% with intact olfaction converted to AD (<i>p</i> = 0.03). The ROC/AUC for prediction of conversion to AD was 0.62. <h3>Conclusions:</h3> Olfactory identification deficit is a useful screening tool for AD-related amnestic disorder, with sensitivity and specificity comparable to other established biomarkers, with benefits such as ease of administration and low cost. Olfactory identification deficit can be utilized to stratify risk of conversion from aMCI to AD and enrich clinical trials of disease-modifying therapy. <h3>Classification of evidence:</h3> This study provides Class III evidence that smell identification (10-item UPSIT subset) accurately identifies patients with amnestic disorders.

The purpose of the study was to provide characterization of Mexican Americans who meet criteria for Alzheimer's disease (AD) and mild cognitive impairment (MCI). For the study, 1,069 participants ages 40 and above who self-identified as either non-Hispanic white (n = 633) or Mexican American (n = 436) were recruited using a community-based participatory research approach. Global cognition was assessed via the Mini-Mental State Examination (MMSE), dementia severity by the Clinical Dementia Rating Scale, and depression via the Geriatric Depression Scale 30-item version. Age, gender, education, ApoE ε4 allele frequency, and diabetic diagnoses were also analyzed. The findings showed that Mexican Americans (normal controls, MCI, and AD) were younger, less highly educated, performed more poorly on the MMSE, endorsed more symptoms of depression, were more likely to be diagnosed with diabetes, and possessed the ApoE ε4 allele less frequently. Age was the only significant risk factor for cognitive dysfunction (AD/MCI) among Mexican Americans (OR = 1.06, 95% CI = 1.03-1.09). Age (B = 0.07, std = 0.02, p < 0.001) and ApoE ε4 presence (B = 0.9, std = 0.4, p = 0.02) were significantly related to increased disease severity. Given the rapidly growing and aging Mexican American population, there is a substantial need for research into cognitive aging, MCI, and AD among this ethnic group. The current findings hold important implications for both clinic and research settings and point to additional research needs.

OBJECTIVE: To determine the physiological adaptations in previously sedentary healthy older men and women (mean age = 68) to a 16-week low-to-moderate-intensity exercise program. DESIGN: Randomized, controlled trial. SETTING: An exercise facility and testing laboratory in a gerontological research institute. PARTICIPANTS: Two-hundred forty-seven community-dwelling older persons free of significant cardiovascular, pulmonary, or uncontrolled metabolic disease, anemia, electrolyte abnormality, resting BP of 165/90 or greater, or chronic disease affecting the ability to exercise on a bicycle. INTERVENTION: Subjects were randomly assigned to either an exercise (n = 166) or attention control group (n = 81). Exercisers trained thrice weekly for 40 minutes on a cycle ergometer (5-minute warm up, 30 minutes at training heart rate (THR), 5-minute cool down). THR was set at 70% of peak heart rate attained on a maximal exercise test (mean = 115 +/- 15). Control subjects attended weekly group talks. Testing took place before and after the program. RESULTS: Peak attained oxygen uptake (VO2max) increased 8.5% in exercisers and decreased slightly in controls (p less than .001) and oxygen uptake at ventilatory threshold (VeT VO2) increased by 3.5% in exercisers and decreased by 3% in controls (p less than .001). This pattern of a greater increase in VO2max than VeT VO2 is different from that seen in young and middle-aged subjects. CONCLUSION: This study demonstrated that a large scale training program is feasible for healthy older people, that physiologic improvements can be measured after 16 weeks of low-to-moderate-intensity training, and that mechanisms of adaptation to exercise may be different in elderly subjects from those in younger ones.