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Background Memory clinics (MC) are institutions specialized in the (differential) diagnostics, treatment, education, management and counseling of diseases related to dementia and their risk stages. In Germany, they have a variety of different organizational forms. Due to the growing diagnostic options in neurodegenerative diseases, the increasing demand for early detection and prediction as well as foreseeable new diagnostic procedures and disease-modifying treatment, it is important to standardize the structural prerequisites and areas of responsibility of MC. Objective The article proposes structural and organizational requirements and procedures and a harmonized mode of operation for MC in Germany. Method Expert consensus of psychiatrists, neurologists and geriatricians from academic and nonacademic institutions. Results The MC should provide the specialist standards of psychiatry and/or neurology. They need to implement the recommendations of the national guidelines on dementia (S3LL) with respect to the (differential) diagnostics and treatment of dementia. With respect to the early detection and prediction of neurodegenerative disorders, they extend beyond the current German guideline standards. In MC, mild cognitive impairment (MCI) is understood as an at-risk or prodromal stage of diseases related to dementia and biomarkers are consistently applied for etiological (early and differential) diagnostics. There is a requirement for close interaction with specialized diagnostic disciplines. Furthermore, MC should also offer comprehensive advice on social and legal issues and provide caregiver support. They should integrate current knowledge from research into care and serve as regional expert centers. Conclusion The MC should implement evidence-based standards in diagnostics and treatment and introduce innovations in the care of patients with cognitive disorders and at-risk and prodromal stages. Their role in the German healthcare system must be strengthened. Suff

Human cognitive processes are highly variable across individuals and are influenced by both genetic and environmental factors. Although genetic variations affect short-term memory in humans, it is unknown whether genetic variability has also an impact on long-term memory. Because prion-like conformational changes may be involved in the induction of long-lasting synaptic plasticity, we examined the impact of single-nucleotide polymorphisms (SNPs) of the prion protein gene (PRNP) on long-term memory in healthy young humans. SNPs in the genomic region of PRNP were associated with better long-term memory performance in two independent populations with different educational background. Among the examined PRNP SNPs, the common Met129Val polymorphism yielded the highest effect size. Twenty-four hours after a word list-learning task, carriers of either the 129MM or the 129MV genotype recalled 17% more information than 129VV carriers, but short-term memory was unaffected. These results suggest a role for the prion protein in the formation of long-term memory in humans

Nadeem Kalak,1 Serge Brand,1,2 Johannes Beck,1 Edith Holsboer-Trachsler,1 M Axel Wollmer1,3 1Psychiatric Clinics of the University of Basel, 2Department of Sport and Health Science, Division of Sport Science, University of Basel, Basel, Switzerland; 3Asklepios Clinic North Ochsenzoll, Asklepios Campus Hamburg, Medical Faculty, Semmelweis University, Hamburg, Germany Background: Poor sleep is a major health concern, and there is evidence that young adults are at increased risk of suffering from poor sleep. There is also evidence that sleep duration can vary as a function of gender and body mass index (BMI). We sought to replicate these findings in a large sample of young adults, and also tested the hypothesis that a smaller gap between subjective sleep duration and subjective sleep need is associated with a greater feeling of being restored.Methods: A total of 2,929 university students (mean age 23.24±3.13 years, 69.1% female) took part in an Internet-based survey. They answered questions related to demographics and subjective sleep patterns.Results: We found no gender differences in subjective sleep duration, subjective sleep need, BMI, age, or feeling of being restored. Nonlinear associations were observed between subjective sleep duration, BMI, and feeling of being restored. Moreover, a larger discrepancy between subjective actual sleep duration and subjective sleep need was associated with a lower feeling of being restored.Conclusion: The present pattern of results from a large sample of young adults suggests that males and females do not differ with respect to subjective sleep duration, BMI, or feeling of being restored. Moreover, nonlinear correlations seemed to provide a more accurate reflection of the relationship between subjective sleep and demographic variables. Keywords: young adults, subjective sleep duration, subjective sleep need, body mass index, Internet-based study

Alzheimer’s disease (AD) is a genetically complex disorder, and several genes related to cholesterol metabolism have been reported to contribute to AD risk. To identify further AD susceptibility genes, we have screened genes that map to chromosomal regions with high logarithm of the odds scores for AD in full genome scans and are related to cholesterol metabolism. In a European screening sample of 115 sporadic AD patients and 191 healthy control subjects, we analyzed single nucleotide polymorphisms in 28 cholesterol-related genes for association with AD. The genes HMGCS2, FDPS, RAFTLIN, ACAD8, NPC2, and ABCG1 were associated with AD at a significance level of P ≤ 0.05 in this sample. Replication trials in five independent European samples detected associations of variants within HMGCS2, FDPS, NPC2, or ABCG1 with AD in some samples (P = 0.05 to P = 0.005). We did not identify a marker that was significantly associated with AD in the pooled sample (n = 2864). Stratification of this sample revealed an APOE-dependent association of HMGCS2 with AD (P = 0.004). We conclude that genetic variants investigated in this study may be associated with a moderate modification of the risk for AD in some samples.