Scientists have identified many new genes associated with better thinking skills following a major worldwide study.
They also found 42 genome-wide loci linked to reaction time, 40 of which are new to science.
Scientists have identified new genes associated with cleverness in a study that may help to explain why certain people have better cognitive function.
The study is said to be the largest genetic study of cognitive function and as a result, they have identified some genetic variations between the persons who wear glasses and un-wearers on the thinking capacity.
Scientists think so. They say that people who wear glasses may be more intelligent than those who don't.
Analyzing the genetic data, scientists found that 148 genome-wide regions associated with a general cognitive function, including 58 genomic sites that hadn't previously been linked with intelligence.
The study is the largest of its kind ever conducted, according to The Guardian, and also found negative correlations between cognitive function and a number of other health problems, including angina, lung cancer and depression.
Professor Ian Deary, director of the University of Edinburgh's Centre for Cognitive Ageing and Cognitive Epidemiology (CCACE) and lead author of the study said in a statement: "Less than a decade ago we were searching for genes related to intelligence with about 3,000 participants, and we found nearly nothing".
However, the researchers said there was no proof of a defined link between the two factors.
According to lead researcher Ian Deary, "We also need to study our results closely to see what they can tell us about the possibility of understanding the declines in cognitive function that happen with illness and in older age", such as Alzheimer's disease. A double win for the short, and long, sighted..
(A&B) The mtDNA level in PARP1+/- chagasic mice. Mice (WT and PARP1+/-) were infected with T. cruzi and monitored at 150 days’ post-infection. Representative gel images (A, n = 3 mice/group) show myocardial levels of 10 kb mtDNA and short 177-bp mtDNA and 96-bp nuDNA (GAPDH) fragments as controls. PCR amplification was performed for 28 cycles. Densitometry analysis was performed on PCR gels representing n? 6 mice/group, and density of the 10 kb mtDNA band, normalized against mtDNA and nuDNA fragments, is presented in B.a&b. (C-H) Effect of PARP1 inhibitor on cardiomyocytes infected with T. cruzi. Cardiac myocytes were infected with T. cruzi in presence or absence of PJ34 for 24 h. RT-qPCR was employed to evaluate the mRNA level for PARP1 and several components of the POLG replisome machinery, and data were normalized to GAPDH mRNA. (I-K) Cardiomyocytes were incubated for 24 with Tc in presence and absence of PJ34. ROS release was measured by an amplex red assay (I). MitoSOX red fluorescence detects mitochondrial O2•? level (J). Ratio of fluorescence intensity of J-monomers (green) to J-aggregates (red) indicates mitochondrial depolarization (K). Data in C-K were acquired by using three biological replicates (duplicate analysis per sample). Data in all bar graphs are plotted as mean value ± SEM, and statistical significance are marked as *WT.Tc vs. WT, and #WT.Tc vs. genetically-modified/infected or infected/PJ34-treated (#p<0.05, ***,###p<0.001).