Reduced ability on cognitive tasks sensitive to frontal lobe damage seems to be associated with a higher risk of psychotic symptoms in AD,43,48 supporting the hypothesis that symptoms such as hallucinations and delusions could be produced by pathological frontal circuitry. Correlation between “frontal” tasks and psychotic symptoms has also been demonstrated in patients with FTD,93 confirming that, independently of the type of dementia, frontal lobe involvement is the main requisite Inhibitors,research,lifescience,medical for the appearance of behavioral manifestations. Generally, however, studies do not explicitly take into account the potential cause-effect relationship between the two types of

manifestations. Namely, although hypothesized, it has never been specifically explored Inhibitors,research,lifescience,medical whether cognitive and noncognitive disorders can both be traced back to the same check details neural damage, or whether behavioral disorders might to some extent represent

a “reaction” to the cognitive deficit. Indeed, it is likely that any limitation of cognitive resources could reduce a patient’s ability to efficiently react to environmental stimulation in order to generate adequate behavioral responses. The memory disorder, to mention the most common example, Inhibitors,research,lifescience,medical typical of AD but also frequent in other types of dementia, might produce such severe functional limitation as to generate reactive depression in amnesic subjects with good insight. Theory of mind and Inhibitors,research,lifescience,medical behavior in

FTD The hypothesis of a direct relationship between cognition and behavior in FTD is now currently proposed in the neuropsychological literature. In particular, it has been proposed that the impairment of “high-level” competences of the frontal lobe might generate behavioral changes, mostly in personality and social conduct. Particular attention has been devoted to the theory of mind (TofM). TofM is the ability to make inferences about others5 mental states, thoughts, and feelings in order to predict and understand their behavior. Inhibitors,research,lifescience,medical TofM is strictly related to the concept of “empathy,” that is, the ability to spread emotions to other people and to understand other people’s emotions. A deficit in TofM, originally proposed to account for developmental disorders in social cognition of subjects affected by pathologies such as autism or Asperger’s syndrome,94,95 could also explain some aspects of the pathological behavior typical of patients Dichloromethane dehalogenase with FTD. The effects of frontal lobe damage on behavior, and in particular of damage in the orbital and ventral regions, have long been known.96 The neurocircuitry of TofM has been delineated by both lesional and functional studies. There is basic agreement in considering the amygdala97 and the orbitofrontal cortex,95 and also the medial prefrontal cortex98 as the anatomical base for TofM (see also ref 99).