Aim: We aimed toevaluatethe psychometric properties of the Subjective Memory Complaints Questionnaire (SMCQ). Methods: The reliability of the SMCQ was evaluated by testing its internal consistency and test-retest reliability. Pearson correlation analyses were performed to assess the concurrent validity. Confirmatory factor analysis was used to evaluate the construct validity. Diagnostic ability for dementia was tested with receiver operator characteristic curve analyses. Results: Cronbach’s α coefficient and intraclass correlation coefficients of the SMCQ were 0.864 and 0.828 (p < 0.001), respectively. The SMCQ scores were significantly correlated with the scores on Camdex Memory Complaint Questionnaire, Seoul Informant Report Questionnaire for Dementia and cognitive tests from the CERAD (Consortium to Establish a Registry for Alzheimer’s Disease) neuropsychological test battery (p < 0.01). The results of confirmatory factor analyses confirmed that the SMCQ consisted of subjective memory complaints (SMC) for general memory and for everyday memory. The SMCQ score discriminated well between nondemented elderly without dementia and those with dementia (p < 0.01). The area under the curve value of the SMCQ was 0.84, indicating that it had high diagnostic ability. Conclusion: The SMCQ was found to be a brief, reliable and valid questionnaire for evaluating SMC. It might be useful for evaluating the cognition of elderly subjects when reliable informants are not available.

The forebrain constitutes the most anterior part of the central nervous system, and is functionally crucial and structurally conserved in all vertebrates. It includes the dorsally positioned telencephalon and eyes, the ventrally positioned hypothalamus, and the more caudally located diencephalon [from rostral to caudal: the prethalamus, the zona limitans intrathalamica (ZLI), the thalamus and the pretectum]. Although antagonizing Wnt proteins are known to establish the identity of the telencephalon and eyes, it is unclear how various subdivisions are established within the diencephalon -a complex integration center and relay station of the vertebrate brain. The conserved forebrain-specific zinc-finger-containing protein Fezl plays a crucial role in regulating neuronal differentiation in the vertebrate forebrain. Here, we report a new and essential role of zebrafish Fezl in establishing regional subdivisions within the diencephalon. First, reduced activity of fezl results in a deficit of the prethalamus and a corresponding expansion of the ZLI. Second, Gal4-UAS-mediated fezl overexpression in late gastrula is capable of expanding the prethalamus telencephalon and hypothalamus at the expense of the ZLI and other fore-and/or mid-brain regions. Such altered brain regionalization is preceded by the early downregulation of wnt expression in the prospective diencephalon. Finally, fezl overexpression is able to restore the anterior forebrain and downregulate wnt expression in Headless-and/or Tcf3 (also known as Tcf7l1a)-deficient embryos. Our findings reveal that Fezl is crucial for establishing regional subdivisions within the diencephalon and may also play a role in the development of the telencephalon and hypothalamus.

The development of vertebrate basal forebrain dopaminergic (DA) neurons requires the conserved zinc finger protein Too Few (Tof͞ Fezl) in zebrafish. However, how Tof͞Fezl regulates the commitment and differentiation of these DA neurons is not known. Proneural genes encoding basic helix-loop-helix transcription factors regulate the development of multiple neuronal lineages, but their involvement in vertebrate DA neuron determination is unclear. Here we show that neurogenin 1 (ngn1), a vertebrate proneural gene related to the Drosophila atonal, is expressed in and required for specification of DA progenitor cells, and when overexpressed leads to supernumerary DA neurons in the forebrain of zebrafish. Overexpression of ngn1 is also sufficient to induce tyrosine hydroxylase expression in addition to the panneuronal marker Hu in nonneural ectoderm. We further show that Tof͞Fezl is required to establish basal forebrain ngn1-expressing DA progenitor domains. These findings identify Ngn1 as a determinant of brain DA neurons and provide insights into how Tof͞Fezl regulates the development of these clinically important neuronal types.neurogenin 1 ͉ pluripotent neural stem cell ͉ neurotransmitter phenotype ͉ commitment and differentiation T he determination of neurotransmitter phenotype is an important aspect of neuronal differentiation, and in this regard, dopaminergic (DA) neurons have attracted considerable attention because of their functional and medical importance (1). Degeneration of substantia nigra DA neurons in humans is a hallmark of Parkinson's disease, and the malfunction of DA neurons in other brain regions is implicated in psychiatric disorders and neuroendocrine dysregulation. Therefore, understanding the determination of DA phenotype and the specification of DA neuronal circuitry may provide mechanistic and therapeutic insights into these disorders. To date, only limited number of known or putative transcriptional regulators, including Pax6, Dlx, Nurr1, Lmx1a, Lmx1b, Msx1, Foggy, and Too Few (Tof͞Fez1), have been implicated in the specification of DA phenotype in vertebrates (2-7, 35). Despite this knowledge, the mechanisms leading to the early commitment of pluripotent neural stem cells to DA lineage remain elusive.The earliest DA neurons in zebrafish are detected at Ϸ24 h postfertilization (hpf) in the basal forebrain (8). They express tyrosine hydroxylase (TH), the rate-limiting enzyme in dopamine synthesis, and dopamine transporter (DAT), a protein involved in dopamine reuptake (9). Later during development, these DA neurons have both ascending and descending projections, and are believed to be homologous to mammalian DA neurons of both the basal forebrain and midbrain (10,11).Through forward genetic analysis, an adult viable zebrafish mutant named too few (tof m808 ) has been isolated that displays selective deficits of basal forebrain DA as well as adjacent serotonergic (5HT) neurons (8). Molecular characterizations have revealed that the too few mutant carries a point mutation that changes Cys-287 t...

Background/Aims: We investigated the demographic influence on the performance of the Revised Hasegawa Dementia Scale (HDS-R) and provided normative data of the HDS-R in the elderly. Methods: The HDS-R was administered to 803 community-dwelling cognitively normal elderly subjects aged 55 years or over. Cognitive disorders and psychiatric disorders were strictly excluded using the CERAD-K assessment packet and the Mini-International Neuropsychiatric Interview. The demographic influence on the performance of the HDS-R was examined using multiple linear regression analyses, and compared with that on the performance of the Mini-Mental Status Examination (MMSE) using the Chow test and t statistics. Overlapping strata were used in developing age-, education- and gender-specific normative data of the HDS-R. Results: Age, education, and gender influenced significantly the performance of the HDS-R, and explained 22.5% of the total score variance. Older age, lower education, and male gender were associated with lower performance of the HDS-R. However, the demographic influence on the HDS-R was much weaker than that on the MMSE (t = 5.578, d.f. = 800, p < 0.001). The normative data of the HDS-R stratified by age (60–69, 70–79, ≧80), education (0–6, 7–12, ≧13), and gender were presented. Conclusions: The HDS-R was more robust to demographic influences than the MMSE, and normative data may contribute to improving further its diagnostic accuracy for dementia.