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Alzheimer's disease (AD) has been associated with increased phosphorylation of the translation initiation factor 2 α  (eIF2 α ) at serine 51. Increased phosphorylation of eIF2 α  alters translational control and may thereby have adverse effects on synaptic plasticity, learning, and memory. To analyze if increased levels of p-eIF2 α  indeed promote AD-related neurocognitive impairments, we crossed 5xFAD transgenic mice with an  eIF 2 α    S 51A  knock-in line that expresses the nonphosphorylatable eIF2 α  variant  eIF 2 α    S 51A . Behavioral assessment of the resulting mice revealed motor and cognitive deficits in 5xFAD mice that were, with the possible exception of locomotor hyperactivity, not restored by the  eIF 2 α    S 51A  allele. Telemetric intracranial EEG recordings revealed no measurable effects of the  eIF 2 α    S 51A  allele on 5xFAD-associated epileptic activity. Microarray-based transcriptome analyses showed clear transcriptional alterations in 5xFAD hippocampus that were not corrected by the  eIF 2 α    S 51A  allele. In contrast to prior studies, our immunoblot analyses did not reveal increased levels of p-eIF2 α  in the hippocampus of 5xFAD mice, suggesting that elevated p-eIF2 α  levels are not a universal feature of AD models. Collectively, our data indicate that 5xFAD-related pathologies do not necessarily require hyperphosphorylation of eIF2 α  to emerge; they also show that heterozygosity for the nonphosphorylatable  eIF 2 α    S 51A  allele has limited effects on 5xFAD-related disease manifestations.

Limited Effects of aneIF2αS51AAllele on Neurological Impairments in the 5xFAD Mouse Model of Alzheimer’s Disease

Limited Effects of aneIF2α^S51AAllele on Neurological Impairments in the 5xFAD Mouse Model of Alzheimer’s Disease