Aim:To evaluate the association of cognitive impairment, depressive mood and sarcopenia among older men living in the veterans retirement community in southern Taiwan Methods: This cross-sectional study recruited 353 men aged 65 years and older. In addition to demographic characteristics, all participants were measured for gait speed, handgrip strength and muscle mass by using bioelectrical impedance analysis (BIA). The diagnosis of sarcopenia was made according to the European Working Group on Sarcopenia in Older People criteria. Slow walking speed was defined as ≤0.8 meter/second. Low muscle strength was defined as the handgrip strength less than 22.5 kg which was adjusted according to Taiwanese norms. A heightadjusted muscle mass of 8.87 kg/m2 from a previous Taiwanese study was defined as low muscle mass. Cognitive function was evaluated by the Mini-Mental State Examination (MMSE), and the Geriatric Depression Scale-15 (GDS-15) was used for screening of depressive symptoms.Results: Among the 353 participants (mean age 82.7 ± 5.3 years), 30.9% (109/353) were classified as sarcopenic. Multivariate logistic regression showed that sarcopenia was independently associated with cognitive impairment (adjusted OR 3.03, 95% CI 1.63-5.65, P < 0.001) and depressive symptoms (adjusted OR 2.25, 95% CI 1.03-4.89, P = 0.04). Conclusions:Sarcopenia was significantly associated with cognitive impairment and depressive symptoms among otherwise healthy older men living in the veterans retirement community. Further outcome study is required to explore the interrelationship of cognition, depressive symptoms and sarcopenia in older adults. Geriatr Gerontol Int 2014; 14 (Suppl. 1): 102-108.

Neurodegenerative diseases are an enormous public health problem, affecting tens of millions of people worldwide. Nearly all of these diseases are characterized by oligomerization and fibrillization of neuronal proteins, and there is great interest in therapeutic targeting of these aggregates. Here, we show that soluble aggregates of α-synuclein and tau bind to plateimmobilized PrP in vitro and on mouse cortical neurons, and that this binding requires at least one of the same N-terminal sites at which soluble Aβ aggregates bind. Moreover, soluble aggregates of tau, α-synuclein and Aβ cause both functional (impairment of LTP) and structural (neuritic dystrophy) compromise and these deficits are absent when PrP is ablated, knocked-down, or when neurons are pre-treated with anti-PrP blocking antibodies. Using an all-human experimental paradigm involving: (1) isogenic iPSC-derived neurons expressing or lacking PRNP, and (2) aqueous extracts from brains of individuals who died with Alzheimer's disease, dementia with Lewy bodies, and Pick's disease, we demonstrate that Aβ, α-synuclein and tau are toxic to neurons in a manner that requires PrP C. These results indicate that PrP is likely to play an important role in a variety of late-life neurodegenerative diseases and that therapeutic targeting of PrP, rather than individual disease proteins, may have more benefit for conditions which involve the aggregation of more than one protein.

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