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Alzheimer's disease (AD) is a neurodegenerative disorder, and no effective treatments are available to treat this disorder. Therefore, researchers have been investigating Hericium erinaceus, or the monkey head mushroom, an edible medicinal mushroom, as a possible treatment for AD. In this narrative review, we evaluated six preclinical and three clinical studies of the therapeutic effects of Hericium erinaceus on AD. Preclinical trials have successfully demonstrated that extracts and bioactive compounds of Hericium erinaceus have potential beneficial effects in ameliorating cognitive functioning and behavioral deficits in animal models of AD. A limited number of clinical studies have been conducted and several clinical trials are ongoing, which have thus far shown analogous outcomes to the preclinical studies. Nonetheless, future research on Hericium erinaceus needs to focus on elucidating the specific neuroprotective mechanisms and the target sites in AD. Additionally, standardized treatment parameters and universal regulatory systems need to be established to further ensure treatment safety and efficacy. In conclusion, Hericium erinaceus has therapeutic potential and may facilitate memory enhancement in patients with AD. [ABSTRACT FROM AUTHOR]

This study examined [Ca.sup.2+] handling mechanisms involved in cardioprotection induced by chronic intermittent hypoxia (CIH) against ischemia-reperfusion (I/R) injury. Adult male Sprague-Dawley rats were exposed to 10% inspired [O.sub.2] continuously for 6 h daily from 3, 7, and 14 days. In isolated perfused hearts subjected to I/R, CIH-induced cardioprotection was most significant in the 7-day group with less infarct size and lactate dehydrogenase release, compared with the normoxic group. The I/R-induced alterations in diastolic [Ca.sup.2+] level, amplitude, time-to-peak, and the decay time of both electrically and caffeine-induced [Ca.sup.2+] transients measured by spectrofluorometry in isolated ventricular myocytes of the 7-day CIH group were less than that of the normoxic group, suggesting an involvement of altered [Ca.sup.2+] handling of the sarcoplasmic reticulum (SR) and sarcolemma. We further determined the protein expression and activity of [sup.45][Ca.sup.2+] flux of SR-[Ca.sup.2+]-ATPase, ryanodine receptor (RyR) and sarcolemmal [Na.sup.+]/[Ca.sup.2+] exchange (NCX) in ventricular myocytes from the CIH and normoxic groups before and during I/R. There were no changes in expression levels of the [Ca.sup.2+]-handling proteins but significant increases in the RyR and NCX activities were remarkable during I/R in the CIH but not the normoxic group. The augmented RyR and NCX activities were abolished, respectively, by PKA inhibitor (0.5 [micro]M KT5720 or 0.5 [micro]M PK[I.sub.14.22]) and PKC inhibitor (5 [micro]M chelerythrine chloride or 0.2 [micro]M calphostin C) but not by [Ca.sup.2+]/calmodulin-dependent protein kinase II inhibitor KN-93 (1 [micro]M). Thus, CIH confers cardioprotection against I/R injury in rat cardiomyocytes by altered [Ca.sup.2+] handling with augmented RyR and NCX activities via protein kinase activation. cardioprotection; intracellular calcium doi:10.1152/ajpcell.00458.2006

Male rats aged 3 months, 12 months and 20 months were subjected to breathing 8% oxygen for 6 hours. Lung preproadrenomedullin (AM) messenger RNA (mRNA) levels were measured by solution hybridization-RNase protection assay while AM was measured by radioimmunoassay. The binding of hypoxia-inducible factor-1[alpha] (HIF-1[alpha]) to DNA was determined by electrophoretic mobility shift. There was an age-related increase in basal levels of preproAM mRNA and AM and of the binding of hypoxia-inducible factor (HIF) to DNA. Upon hypoxic stimulation, HIF binding to DNA increased in the young and middle-aged rats, but not in the old rats. AM gene expression increased in response to hypoxia in rats of all ages, but the increase was much less in the old rats. AM peptide levels in the lung decreased with age in hypoxia. In a separate experiment, male rats aged 3 months and 20 months were subjected to hypoxia as described above. PreproAM, calcitonin receptor-like receptor (CRLR), receptor activity modifying protein (RAMP) mRNA, HIF-1 and peptidyl-glycine-amidating monooxygenase (PAM) mRNA levels were measured by reverse transcription--polymerase chain reaction. All except PAM showed a decrease in basal levels and a diminished response to hypoxia in the old rats. Polysome profiling demonstrated decreases in the percentages of translatable preproAM mRNA in response to hypoxia, with a greater decrease in the old than the young rats. It is concluded that an agedependent decrease in the hypoxic response of the AM system in the lung was associated with high basal levels of H1F activity and AM expression in the old rats, and a lower proportion of translatable preproAM mRNA in the old rats in response to hypoxia. Thus, the HIF-AM pathway may be impaired in the aged lung, and other mechanisms may be present to maintain an AM response to hypoxia.

The present study determined [Ca.sup.2+] handling in the hearts of rats subjected to chronic hypoxia (CH). Spectrofluorometry was used to measure intracellular [Ca.sup.2+] concentration ([[[Ca.sup.2+]].sub.i]) and its responses to electrical stimulation, caffeine, and isoproterenol in myocytes from the right ventricle of rats breathing 10% oxygen for 1, 3, 7, 14, 21, 28, and 56 days and age-matched controls. The protein expression of sarco(endo)plasmic reticulum [Ca.sup.2+]-ATPase (SERCA) and its ryanodine receptor (RyR) were measured. The uptake of [sup.45][Ca.sup.2+] by SERCA, release by RyR, and extrusion by [Na.sup.+]/[Ca.sup.2+] exchange (NCX) were determined. It was found that [Ca.sup.2+] homeostasis and [Ca.sup.2+] responses to [beta]-adrenoceptor stimulation reached a new equilibrium after 4 wk of CH. [Ca.sup.2+] content in the sarcoplasmic reticulum (SR) was reduced, but cytosolic [Ca.sup.2+] remained unchanged after CH. Expression of SERCA and its [Ca.sup.2+] uptake, [Ca.sup.2+] release via RyR, and NCX activity were suppressed by CH. The results indicate impaired [Ca.sup.2+] handling, which may be responsible for the attenuated [Ca.sup.2+] responses to [beta]-adrenoceptor stimulation in CH. intracellular calcium ion concentration; calcium-adenosine-triphosphatase; ryanodine receptor; sodium/calcium exchange; sarcoplasmic reticulum; [beta]-adrenoceptor; chronic hypoxia