Among all the clinical indications for which radiologists, nuclear medicine physicians,
neurologists, neurosurgeons, psychiatrists (and others examining disorders of
the brain) order and read brain PET scans, demand is greatest for those pertaining
to dementia and related disorders. This demand is driven by the sheer prevalence of
those conditions, coupled with the fact that the differential diagnosis for causes of
cognitive impairment is wide and often difficult to distinguish clinically.
Population Screening Mass genetic screening programs require tests of high enough sensitivity and specificity to be cost-effective. An effective screening program should fulfill the following criteria: that the tested disorder is prevalent and serious; that it can be influenced presymptomatically through lifestyle changes, screening, or medications; and that identification of risk does not result in undue discrimination or harm.
Brain morphology is in constant change from the very beginning of the neurodevelopment in human beings. The characterization of the brain morphology and its biological implications on a specific subject is a complex task which requires efficient computational approaches. Radiology has traditionally assessed the main brain changes in different alterations from a macroscopic point of view, thus, not considering subtle changes as a results of neuronal plasticity.
DNA testing is performed by mutational analysis or linkage studies in individuals at risk for a genetic disorder known to be present in a family. Mass screening programs require tests of high sensitivity and specificity to be costeffective. Prerequisites for the success of genetic screening programs include the following: that the disorder is potentially serious; that it can be influenced at a presymptomatic stage by changes in behavior, diet, and/or pharmaceutical manipulations; and that the screening does not result in any harm or discrimination.
Huntington’s disease (HD) is a progressive neurodegenerative disorder
characterized by multifarious dysfunctional alterations including mitochon-drial impairment. In the present study, the formation of inclusions caused
by the mutation of huntingtin protein and its relationship with changes in
energy metabolism and with pathological alterations were investigated both
in transgenic and 3-nitropropionic acid-treated mouse models for HD.
The S100 proteins are 10–12 kDa EF-hand proteins that act as central reg-ulators in a multitude of cellular processes including cell survival, prolifera-tion, differentiation and motility. Consequently, many S100 proteins are
implicated and display marked changes in their expression levels in many
types of cancer, neurodegenerative disorders, inflammatory and autoim-mune diseases.