"Dynamisches 201TIDD-SPECT zur Erfassung der zeitlichen und räumlichen Ausbreitung eines ischämischen Schadens in der Akutphase des experimentellen Schlaganfalls"

Otto-von-Guericke-Universität Magdeburg, Fakultät für Naturwissenschaften, Dissertation, 2016von Master of Science Franziska StöberLiteraturverzeichnis: Seite 102-12

Metabolic brain networks in aging and preclinical Alzheimer's disease.

Metabolic brain networks can provide insight into the network processes underlying progression from healthy aging to Alzheimer's disease. We explore the effect of two Alzheimer's disease risk factors, amyloid-β and ApoE ε4 genotype, on metabolic brain networks in cognitively normal older adults (N = 64, ages 69-89) compared to young adults (N = 17, ages 20-30) and patients with Alzheimer's disease (N = 22, ages 69-89). Subjects underwent MRI and PET imaging of metabolism (FDG) and amyloid-β (PIB). Normal older adults were divided into four subgroups based on amyloid-β and ApoE genotype. Metabolic brain networks were constructed cross-sectionally by computing pairwise correlations of metabolism across subjects within each group for 80 regions of interest. We found widespread elevated metabolic correlations and desegregation of metabolic brain networks in normal aging compared to youth and Alzheimer's disease, suggesting that normal aging leads to widespread loss of independent metabolic function across the brain. Amyloid-β and the combination of ApoE ε4 led to less extensive elevated metabolic correlations compared to other normal older adults, as well as a metabolic brain network more similar to youth and Alzheimer's disease. This could reflect early progression towards Alzheimer's disease in these individuals. Altered metabolic brain networks of older adults and those at the highest risk for progression to Alzheimer's disease open up novel lines of inquiry into the metabolic and network processes that underlie normal aging and Alzheimer's disease

Three-dimensional mouse brain cytoarchitecture revealed by laboratory-based x-ray phase-contrast tomography

Studies of brain cytoarchitecture in mammals are routinely performed by serial sectioning of the specimen and staining of the sections. The procedure is labor-intensive and the 3D architecture can only be determined after aligning individual 2D sections, leading to a reconstructed volume with non-isotropic resolution. Propagation-based x-ray phase-contrast tomography offers a unique potential for high-resolution 3D imaging of intact biological specimen due to the high penetration depth and potential resolution. We here show that even compact laboratory CT at an optimized liquid-metal jet microfocus source combined with suitable phase-retrieval algorithms and a novel tissue preparation can provide cellular and subcellular resolution in millimeter sized samples of mouse brain. We removed water and lipids from entire mouse brains and measured the remaining dry tissue matrix in air, lowering absorption but increasing phase contrast. We present single-cell resolution images of mouse brain cytoarchitecture and show that axons can be revealed in myelinated fiber bundles. In contrast to optical 3D techniques our approach does neither require staining of cells nor tissue clearing, procedures that are increasingly difficult to apply with increasing sample and brain sizes. The approach thus opens a novel route for high-resolution high-throughput studies of brain architecture in mammals

Suicide after reception into prison: a case-control study examining differences in early and late events

Objective: Prisoners constitute a high-risk group for suicide, with suicide rates about 5 to 8 times higher than in the general population. The first weeks of imprisonment are a particularly vulnerable time, but there is limited knowledge about the risk factors for either early or late suicide events. Methods: Based on a national total sample of prison suicides in Germany between 2005 and 2017, suicides within the first 2 (4 and 8) weeks after reception into prison were matched by age and penalty length with cases that occurred later. Factors that potentially influence the timing of suicide were investigated. Results: The study has shown that 16.7% (31.5%) of all 390 suicides in German prisons occurred within the first two weeks (two months) of imprisonment. Factors that facilitate adaptation to the prison environment (e.g. prior prison experience) were negatively associated with early suicide events. Factors that hindered the adaptation process (e.g. withdrawal from illicit drugs) were observed more frequently in early suicide events than in late ones. These factors are active at different times of imprisonment. Conclusion: At reception, particular attention should be paid to the following factors associated with early suicide events: widowed marital status, lack of prison experience, and drug dependency

Genetically Induced Retrograde Amnesia of Associative Memories After Neuroplastin Ablation

BACKGROUND: Neuroplastin cell recognition molecules have been implicated in synaptic plasticity. Polymorphisms in the regulatory region of the human neuroplastin gene (NPTN) are correlated with cortical thickness and intellectual abilities in adolescents and in individuals with schizophrenia. METHODS: We characterized behavioral and functional changes in inducible conditional neuroplastin-deficient mice. RESULTS: We demonstrate that neuroplastins are required for associative learning in conditioning paradigms, e.g., two-way active avoidance and fear conditioning. Retrograde amnesia of learned associative memories is elicited by inducible neuron-specific ablation of Nptn gene expression in adult mice, which shows that neuroplastins are indispensable for the availability of previously acquired associative memories. Using single-photon emission computed tomography imaging in awake mice, we identified brain structures activated during memory recall. Constitutive neuroplastin deficiency or Nptn gene ablation in adult mice causes substantial electrophysiologic deficits such as reduced long-term potentiation. In addition, neuroplastin-deficient mice reveal profound physiologic and behavioral deficits, some of which are related to depression and schizophrenia, which illustrate neuroplastin’s essential functions. CONCLUSIONS: Neuroplastins are essential for learning and memory. Retrograde amnesia after an associative learning task can be induced by ablation of the neuroplastin gene. The inducible neuroplastin-deficient mouse model provides a new and unique means to analyze the molecular and cellular mechanisms underlying retrograde amnesia and memory

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