The Human Genome project , a deep look into who you are and what you may possibly become, the link between the past and degenerative conditions. what are we discovering Gene by Gene ? the science and tech required to study the genome is relatively complicated but comprehension of the literature is not, with a good dictionary an American encyclopedia of health and passion for understanding,  the scientific terminology  will be like riding a bike. this particular article for me aimed at a specific place and condition the frontotemporal lobar degeneration’  its only the recognition of the gene which causes or may be attributed to such conditions as Alzheimer disease, sporadic Creutzfeldt-Jakob disease, Huntington disease-like syndrome, and other nonspecific neurodegenerative disease. Now most people will have had experience with these conditions in their family myself included , and modern studies “say” this may be an inherited condition, I beg to differ as natural holistic Administers  have found the proper science of natural herbal healthcare and wellness, in essence  prevention to body degeneration.  the Frontotemporal lobar is well the 6th chakra or area of the 3rd eye!
alpha lobeany effects to this area should be taken seriously and if you have a genetic predisposition or a degenerative C9orf72 Genome this information is valuable to you, with age comes the chance you may suffer and its not you who will feel the pain or learn resentment it will be your children and grand children or you may just want to be healthy enough that they don’t toss you away in a nursing home.      alpha lobe 2    
the Brain , and the Blood life’s true Potion alpha lobe 3

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Large C9orf72 Hexanucleotide Repeat Expansions Are Seen in Multiple Neurodegenerative Syndromes and Are More Frequent Than Expected in the UK Population

Hexanucleotide repeat expansions in C9orf72 are a major cause of frontotemporal lobar degeneration (FTLD) and amyotrophic lateral sclerosis (ALS). Understanding the disease mechanisms and a method for clinical diagnostic genotyping have been hindered because of the difficulty in estimating the expansion size. We found 96 repeat-primed PCR expansions: 85/2,974 in six neurodegenerative diseases cohorts (FTLD, ALS, Alzheimer disease, sporadic Creutzfeldt-Jakob disease, Huntington disease-like syndrome, and other nonspecific neurodegenerative disease syndromes) and 11/7,579 (0.15%) in UK 1958 birth cohort (58BC) controls. With the use of a modified Southern blot method, the estimated expansion range (smear maxima) in cases was 800–4,400. Similarly, large expansions were detected in the population controls. Differences in expansion size and morphology were detected between DNA samples from tissue and cell lines. Of those in whom repeat-primed PCR detected expansions, 68/69 were confirmed by blotting, which was specific for greater than 275 repeats. We found that morphology in the expansion smear varied among different individuals and among different brain regions in the same individual. Expansion size correlated with age at clinical onset but did not differ between diagnostic groups. Evidence of instability of repeat size in control families, as well as neighboring SNP and microsatellite analyses, support multiple expansion events on the same haplotype background. Our method of estimating the size of large expansions has potential clinical utility. C9orf72-related disease might mimic several neurodegenerative disorders and, with potentially 90,000 carriers in the United Kingdom, is more common than previously realized.

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