Frank hypothyroidism is known to induce neurological and mental dysfunction. The aim of this study was to assess selected neuropsychological and behavioral features by means of standardized tests in a group of 14 patients with subclinical hypothyroidism who were free from neuropsychological complaints and to evaluate the possible effects of L-thyroxine treatment on their performance. Patients were submitted to the Crown and Crisp Experiential Index and to the Wechsler Memory Scale; their ratings on the neurobehavioral tests and their thyroid hormone profile were compared to those of a control group of 50 age-and sex-matched subjects. Comparison was also carried out between pretreatment ratings and those obtained following a 6-month L-thyroxine course (0.1-0.15 mg/day). The Wechsler Memory Scale ratings showed a significant impairment in patients' memory-related abilities [memory quotient (MQ) = 89.1 _+ 2.9; P = 0.002 (patients versus controls)] ; the Crown and Crisp Experiential Index ratings demonstrated moderate differences between untreated patients and controls with respect to hysteria (P=0.03), anxiety (P=0.05), somatic complaints (P = 0.0005), and depressive features (P= 0.002) scales; the total score was also significantly higher (42.0 + 3.8 ; P = 0.005). After L-thyroxine treatment the patients' performances showed an improvement in memory skills, as evaluated by the Wechsler Memory Scale [MQ= 99.9 + 4.0; P= 0.002 (treated versus untreated)] ; somatic complaints (P=0.02) and obsessionality (P = 0.04) ratings and the Crown and Crisp Experiential Index total score (P = 0.04) significantly decreased with respect to untreated patients. The remarkable effects of L-thyroxine treatment observed in the present study indicate that patients with subAbbreviations: TSH=thyrotropin; TRH=thyrotropin-releasing hormone; L-T4=levothyroxine; TT4=total thyroxine; FT 4=free thyroxine, TTa =total 3,5,3'-triiodothyronine; FT3=free 3,5,3'-triiodothyronine, WMS=Wechsler Memory Scale; CCEI = Crown and Crisp Experiential Index clinical hypothyroidism may require early therapy to provide specific treatment for their neuropsychological alterations and to avoid progression toward frank hypothyroidism.Frank hypothyroidism has long been known to induce major neurological and psychological dysfunction [14] ; in particular, depression, mania, and dementia or dementialike features may occur. Moreover, it has been reported to occur more commonly in lithium-treated patients suffering from bipolar affective illness than in unselected psychiatric patients [22] ; a high prevalence of hypothyroidism has also been reported in a subgroup with the "rapid cycling" form [4,6]. Several studies also suggest that subclinical hypothyroidism, an apparently asymptomatic state with normal serum thyroid hormone and increased thyrotropin (TSH) concentrations [10], may be associated with some psychiatric disorders, such as bipolar affective illness [6,16,17]. There is growing evidence for the presence of metabolic and cardiovascular abnormalities rather simil...

Alzheimer’s disease (AD) manifests with progressive memory loss and spatial disorientation. Neuropathological studies suggest early AD pathology in the entorhinal cortex (EC) of young adults at genetic risk for AD (APOE ε4-carriers). Because the EC harbors grid cells, a likely neural substrate of path integration (PI), we examined PI performance in APOE ε4-carriers during a virtual navigation task. We report a selective impairment in APOE ε4-carriers specifically when recruitment of compensatory navigational strategies via supportive spatial cues was disabled. A separate fMRI study revealed that PI performance was associated with the strength of entorhinal grid-like representations when no compensatory strategies were available, suggesting grid cell dysfunction as a mechanistic explanation for PI deficits in APOE ε4-carriers. Furthermore, posterior cingulate/retrosplenial cortex was involved in the recruitment of compensatory navigational strategies via supportive spatial cues. Our results provide evidence for selective PI deficits in AD risk carriers, decades before potential disease onset.

Alzheimer's disease (AD) manifests with progressive memory loss and spatial disorientation. Neuropathological studies suggest early AD pathology in the entorhinal cortex (EC) of young adults at genetic risk for AD (APOE ϵ4-carriers). Because the EC harbors grid cells, a likely neural substrate of path integration (PI), we examined PI performance in APOE ϵ4-carriers during a virtual navigation task. We report a selective impairment in APOE ϵ4-carriers specifically when recruitment of compensatory navigational strategies via supportive spatial cues was disabled. A separate fMRI study revealed that PI performance was associated with the strength of entorhinal grid-like representations, suggesting grid cell dysfunction as a mechanistic explanation for PI deficits in APOE ϵ4-carriers. Furthermore, retrosplenial cortex was involved in the recruitment of compensatory navigational strategies via supportive spatial cues. Our results provide evidence for selective PI deficits in AD risk carriers, decades before potential disease onset.

No abstract

Free- radicals (Oxygen and Nitrogen species) are formed in mitochondria during the oxidative phosphorylation. Their high reactivity, due to not-engaged electrons, leads to an increase of the oxidative stress. This condition affects above all the brain, that usually needs a large oxygen amount and in which there is the major possibility to accumulate “Reacting Species.” Antioxidant molecules are fundamental in limiting free-radical damage, in particular in the central nervous system: the oxidative stress, in fact, seems to worsen the course of neurodegenerative diseases. The aim of this review is to sum up natural antioxidant molecules with the greatest neuroprotective properties against free radical genesis, understanding their relationship with the Central Nervous System.