Cigarette smoking and thinning of the brain's cortex.

Cigarette smoking is associated with cognitive decline and dementia, but the extent of the association between smoking and structural brain changes remains unclear. Importantly, it is unknown whether smoking-related brain changes are reversible after smoking cessation. We analyzed data on 504 subjects with recall of lifetime smoking data and a structural brain magnetic resonance imaging at age 73 years from which measures of cortical thickness were extracted. Multiple regression analyses were performed controlling for gender and exact age at scanning. To determine dose-response relationships, the association between smoking pack-years and cortical thickness was tested and then repeated, while controlling for a comprehensive list of covariates including, among others, cognitive ability before starting smoking. Further, we tested associations between cortical thickness and number of years since last cigarette, while controlling for lifetime smoking. There was a diffuse dose-dependent negative association between smoking and cortical thickness. Some negative dose-dependent cortical associations persisted after controlling for all covariates. Accounting for total amount of lifetime smoking, the cortex of subjects who stopped smoking seems to have partially recovered for each year without smoking. However, it took ~25 years for complete cortical recovery in affected areas for those at the mean pack-years value in this sample. As the cortex thins with normal aging, our data suggest that smoking is associated with diffuse accelerated cortical thinning, a biomarker of cognitive decline in adults. Although partial recovery appears possible, it can be a long process.

Childhood cognitive ability accounts for associations between cognitive ability and brain cortical thickness in old age.

Associations between brain cortical tissue volume and cognitive function in old age are frequently interpreted as suggesting that preservation of cortical tissue is the foundation of successful cognitive aging. However, this association could also, in part, reflect a lifelong association between cognitive ability and cortical tissue. We analyzed data on 588 subjects from the Lothian Birth Cohort 1936 who had intelligence quotient (IQ) scores from the same cognitive test available at both 11 and 70 years of age as well as high-resolution brain magnetic resonance imaging data obtained at approximately 73 years of age. Cortical thickness was estimated at 81 924 sampling points across the cortex for each subject using an automated pipeline. Multiple regression was used to assess associations between cortical thickness and the IQ measures at 11 and 70 years. Childhood IQ accounted for more than two-third of the association between IQ at 70 years and cortical thickness measured at age 73 years. This warns against ascribing a causal interpretation to the association between cognitive ability and cortical tissue in old age based on assumptions about, and exclusive reference to, the aging process and any associated disease. Without early-life measures of cognitive ability, it would have been tempting to conclude that preservation of cortical thickness in old age is a foundation for successful cognitive aging when, instead, it is a lifelong association. This being said, results should not be construed as meaning that all studies on aging require direct measures of childhood IQ, but as suggesting that proxy measures of prior cognitive function can be useful to take into consideration.

Word priming with brief multiple presentation technique: preservation in amnesia.

Many studies have shown relative preservation of word priming in subjects with mild amnesia, but some decrease in severe amnesia. This calls into question the degree of separation between implicit and explicit memory. Possible contamination of implicit memory tasks by impaired explicit memory strategies might be obscuring the actual dissociation between the two memory systems. We have developed a method of circumventing explicit memory contamination by using brief duration repeated primes below the awareness threshold of subjects. We have used this approach to evaluate the status of word priming in densely amnesic subjects. One group of amnesic subjects with alcoholic Korsakoff's syndrome and one group of normal elderly control subjects were tested for word priming on a speeded category membership decision task. Implicit or explicit encoding procedures were used in three different experiments. Results demonstrated that brief multiple presentation of words can offer a means of producing word priming in the absence of explicit recognition or recall of the primed words in both amnesic subjects and normal elderly control subjects. Moreover, there was no significant difference in the magnitude of the priming effect between these groups in the three experiments. These findings show that amnesic subjects can exhibit normal levels of word priming. They also suggest that amnesics retain the capacity to encode, store and retrieve information implicity, e.g. unintentionally.

CM-gag, a transposable-like element reiterated in the genome of Culex pipiens mosquitoes, contains only a gag gene.

CM-gag elements constitute an homogeneous family of sequences that are reiterated in the genome of Culex pipiens strains from different continents. Apparently complete 1.75 kb CM-gag copies are flanked by target-site duplications and have a polyadenylation signal near their 3' end. They potentially contain a unique gene encoding a putative protein that displays homologies with nucleic acid binding proteins and the gag polypeptide of retroviruses and retrotransposons, but that does not encode a reverse transcriptase. CM-gag elements are similar in their genetic organization to the telomeric transposable sequences Het-A from Drosophila melanogaster, but Southern-hybridization patterns indicate that the former are more probably dispersed in various areas of the mosquito genome. The homogeneity of CM-gag copies that are distributed worldwide suggests that they have most probably been amplified recently. Furthermore, selective constraints against amino acid changes have been acting on these sequences, suggesting that they need to encode the gag-like protein to be incorporated into the chromosomes.

Characterization of the unlinked 16S rDNA and 23S-5S rRNA operon of Wolbachia pipientis, a prokaryotic parasite of insect gonads.

The rRNA-encoding genes (rDNAs) have been cloned and characterized from Wolbachia pipientis (Wp), the gonadial bacteria-like parasite of the mosquito Culex pipiens (Cp) and the moth Ephestia cautella (Ec). In Wp from both insect species the rDNAs are organized in a way which appears to be very unusual. The rRNAs are encoded by two unlinked transcription units, each present in a single copy per genome. One contains the 16S rDNA only, while the other is an operon encoding both the 23S and 5S rDNAs. Each transcription unit contains two putative upstream promoters, and downstream a Rho-independent terminator. The 16S rDNA, as well as the 23S-5S rRNA operon are not linked to any tRNA-encoding sequence and lack the antitermination boxes which are usually present immediately downstream from eubacterial promoters of rDNAs. Wp infecting Ec and Cp are highly similar taking as criteria the rDNAs and their flanking sequences. However, it clearly appears that each insect species harbours a different and specific Wp strain, or even subspecies. Phylogenetic relationships deduced from the complete sequences of their rDNAs undoubtedly confirm that Wp from Cp and Ec belong to the alpha-group of Proteobacteria, and are closely related to the Rickettsia.

Endogenous L-dopa in the rat dorsal vagal complex: an immunocytochemical study by light and electron microscopy.

The aim of this work was to examine L-DOPA immunoreactivity (L-DOPA-IR) in the dorsal vagal complex (DVC) of the rat medulla oblongata containing A2/C2 catecholaminergic cell groups, in order to further evaluate the previously proposed hypothesis that various pools of endogenous L-DOPA could be immunocytochemically demonstrated in the mammalian brain. For this purpose, L-DOPA-IR was studied in DVC in comparison with both some other catecholaminergic areas and dopamine immunoreactivity (DA-IR) on adjacent sections of the same brain, by using specific antibodies against glutaraldehyde conjugated L-DOPA and DA. Also, the first preliminary observations of L-DOPA-IR in DVC neurons at the ultrastructural level are reported. The following main results were obtained: (1) bright, intense and homogeneous L-DOPA staining was found in perikarya and proximal neuronal processes situated within the rostrocaudal extension of the DVC; (2) this staining pattern was readily distinct from weak and heterogeneous DA staining; (3) an inverse L-DOPA/DA staining pattern ratio was identified between the DVC and the mesencephalon; (4) L-DOPA-IR at electron microscopic level was roughly similar to that previously observed for DA-IR in mesencephalic cells and their presumptive projections. Although some discrepancies were noticed between L-DOPA staining and data from the literature on tyrosine hydroxylase labeling, our results could not invalidate the hypothesis that, among high L-DOPA/DA ratio containing neurons, some cells in the DVC may contain only L-DOPA.