Beta-amyloid precursor protein-deficient mice show reactive gliosis and decreased locomotor activity

Article Abstract:

Mice homozygous for the beta-amyloid precursor protein (APP) were viable and fertile, but mutant mice weighed 15%-20% less than wild-type controls. Neurological evaluation of homozygous mice revealed decreased locomotor activity and forelimb grip strength, indicating impaired neuronal and muscular function. They also exhibited gliosis at 14 weeks of age, enforcing previous result that misprocessed APP leads to impaired neuronal function.

Genetic aspects, Alzheimer's disease, Mice, Mice (Rodents)

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Environmental enrichment reduces A-beta levels and amyloid deposition in transgenic mice

Article Abstract:

Studies provide evidence that environmental enrichment leads to reductions in steady-state levels of cerebral amyloid-beta peptides and amyloid deposition and selective upregulation in levels of specific transcripts in brains of trangenic mice. The enzymatic activity of an amyloid-beta degrading endopeptidase, nephrilysin, is elevated in the brains of 'enriched' mice and inversely correlated with amyloid burden.

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Nuclear inclusions in glutamine repeat disorders: are they pernicious, coincidental, or beneficial?

Article Abstract:

The incidence of neurodegenerative diseases such as Huntington's disease, spinocerebellar ataxias (SCA) and spinocerebellar muscular atrophy involves the hypothesis that glutamine expansions cause the diseases by the gain of toxic function. The diseases have a common characteristic neuron degeneration and that nuclear translocation of polyglutamine-expanded proteins are capable of initiating pathogenesis.

Cerebellar ataxia, Physiological aspects, Nervous system, Huntington's chorea, Huntington's disease, Nerve degeneration, Glutamine

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