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Early and focal atrophy of medial temporal lobes on magnetic resonance imaging (MRI) in patients with Alzheimer disease (AD) can be measured in several ways.
In 20 patients with probable Alzheimer disease and 29 cognitively normal elderly medial temporal lobe atrophy (MTA) was measured by volumetry using manual tracing of the hippocampus. The volume of the hippocampus was also rated into five categories expressed as MTA scores ranging from 0 (no atrophy) to 4 (severe atrophy) using a simple and quick semiquantitative method according to the published combined widths or the height of selected three mediotemporal structures.
In comparison to controls, AD patients had significantly smaller volume of either hippocampus (median volume of the hippocampus Hipp dx: 1,81 vs 2,23 p=0,001; Hipp sin: 1,60 vs 2,14 p=0,003; Hipp bilat: 3,40 vs 4,31 p=0,0004). The total MTA score of both sides were significantly higher in AD patients (median 4) than that in controls (median 1) (p=0,0004). Nearly 60 % cognitively normal seniors had the MTA score ≤ 0,5. A similar proportion of patients with AD (65 %) had the MTA score ≥ 2.
Hippocampal loss of tissue can be detected by visual rating and volumetry on MRI in patients with AD. Visual MTA rating is the easier and quicker method than more accurate and time consuming volumetry to support the diagnosis of AD on the brain MR imaging.
The project was supported by CNS MSMT 1M0517 and VZ MZČR MZ0PCP2005.
Research into mechanisms of interaction between growth and inhibitory proteins of the CNS and behavioral expressions of healthy and disordered brain is one of the contemporary topics. A knockdown model with decreased expression of Nogo-A protein in neurons was developed on the genetic background of Sprague-Dawley wildtypes. Disruption of this inhibitory factor was hypothesized to result in behavioral abnormalities, which were studied both in young, middle age (6 months) and aged (12 months) rats.
Animals were tested in a battery of Carousel maze variants with various demands for segregation of spatial information and flexibility; animals avoided an unmarked sector of either stable or rotating arena; moreover the sector could be defined in room- or arena-frame. A shortened Carousel maze battery and Morris water maze (MWM) including one- trial matching-to-place and reversal configurations was used.
Nogo-A-deficient rats were impaired in the final phases of the Carousel maze battery but their spatial working memory tested in the MWM was intact. Middle-aged and aged groups were differently affected in the battery, but deficits in young animals were observed not to be worsened with ageing. Concept of multidirectional age-related alterations in this animal model is further supported by biochemical brain changes.
Nogo-A-deficient rats may serve as an extremely useful model of neurodevelopmental deficit, which may manifest by behavioral changes accessible to phenotyping and in-depth analysis. Relevance of this approach for animal models of neuropsychiatric models will be discussed.
It seems that schizophrenia may arise from abnormal neurodevelopment due to aberrant neuron formation and migration and that deletion of Nogo-A (a myelin associated inhibitor of regenerative fiber growth) may lead to schizophrenia-like abnormalities in animal model. Our previous studies reported a high sensitivity of lateral analyses to reveal subtle links and recommended to apply them to validate animal models of diseases accompanied by alterations in brain asymmetry.
Expressions of N-methyl-D-aspartate receptor subunits (NR1, NR2A, NR2B) and activities of subunits-associated synthases of nitric oxide (nNOS, eNOS, iNOS) were evaluated in the right and left cortex of young or old Nogo-A deficient rats.
In young controls, no marked laterality was observed in subunits/synthases excepting iNOS but correlation analyses supported links among some subunits, synthases or subunits - synthases. Drops in NR1 (bilaterally) and in NR2B (in the right side) or asymmetrical alterations in NR1 - nNOS pathway were observed in old controls. In young Nogo-A deficient rats, the increase in iNOS (in the left side) and the disruption in left NR1 - right nNOS or in right NR2A - right eNOS pathways were found. And finally in old Nogo-A deficient animals, we observed the increase in NR1 (bilaterally) and in positive correlation between right eNOS - right iNOS.
Although some changes in subunits/synthases observed in people with schizophrenia were not found in Nogo-A deficient rats, some alterations in laterality support the validity of this model.
The study was supported by MSMT (1M0517) and MZCR (MZ0PCP2005) projects.