Disease relevance of Pick1

• Neurofibrillary tangles (NFT) composed of the microtubule-associated protein tau are prominent in Alzheimer disease (AD), Pick disease, progressive supranuclear palsy (PSP) and corticobasal degeneration (CBD) [1].
• This cholesterol turnover across the brain is increased in neurodegenerative disorders such as Alzheimer's disease and Niemann-Pick type C disease [2].
• We investigated whether up-regulation of L-PGDS is either unique to Krabbe's disease or is a more generalized phenomenon in lysosomal storage disorders (LSDs), using LSD mouse models of Tay-Sachs disease, Sandhoff disease, GM(1) gangliosidosis and Niemann-Pick type C1 disease [3].
• The BALB/c mouse model of Niemann-Pick type C disease exhibits similar neuropathological features to the human condition, including cerebral atrophy, demyelination of the corpus callosum, and degeneration of cerebellar Purkinje cells [4].
• Niemann Pick disease is a family of autosomal recessive disorders characterized by cholesterol accumulation [5].

Psychiatry related information on Pick1

• They also stained, in the same manner, Pick bodies in Pick's disease, and neurofibrillary tangles and neuropil threads in various tangle-forming neurologic diseases [6].

High impact information on Pick1

• NFT and Pick-body-like neuronal lesions occurred in the amygdala, septal nuclei, pre-optic nuclei, hypothalamus, midbrain, pons, medulla, deep cerebellar nuclei and spinal cord, with tau-immunoreactive pre-tangles in the cortex, hippocampus and basal ganglia [1].
• Localization of Niemann-Pick C1 protein in astrocytes: implications for neuronal degeneration in Niemann- Pick type C disease [7].
• Niemann-Pick type C disease and intracellular cholesterol trafficking [8].
• Previous reports indicated that resident macrophages produced low or nondetectable quantities of H2O2 (1-10 nmol H2O2/mg resident macrophage protein) when measured by the phenol red assay described by Pick and Mizel [5] [9].
• Mutant mice with Niemann-Pick type C disease were treated with the peroxisomal inducer perfluorooctanoic acid, which increased peroxisomal beta-oxidation and catalase activity to the same level as in control mice [10].

Biological context of Pick1

• It appears that in Niemann-Pick type C disease treatment with appropriate peroxisomal inducers restores basic cellular functions, indicating a relationship between peroxisomes and cholesterol homeostasis, and thereby may effectively interfere with the development of the disease [10].
• A modifier of Niemann Pick C 1 maps to mouse chromosome 19 [11].

Anatomical context of Pick1

• Flow cytometry was performed to evaluate the effect on peritoneal macrophage survival and phagocytic function and the Pick test was used to determine peroxide production in order to estimate toxicity and potential impairment of macrophage function caused by the chemicals [12].

References