ArticleCurrent biology : CB2018
The Tyrosine Phosphatase STEP Is Involved in Age-Related Memory Decline.
Article in Current biology : CB, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 30 citations in OpenAlex.
- Capsosiphon fulvescens glycopeptides restore synaptic plasticity and mitigate cognitive decline via calcineurin regulation in aged hippocampus.European journal of nutrition · 2025Article
- Examining the effects of extremely low-frequency magnetic fields on cognitive functions and functional brain markers in aged mice.Scientific reports · 2025Article
- VEGFD signaling balances stability and activity-dependent structural plasticity of dendrites.Cellular and molecular life sciences : CMLS · 2024Article
- Targeting protein phosphatases in cancer immunotherapy and autoimmune disorders.Nature reviews. Drug discovery · 2023Review
- Age-related memory vulnerability to interfering stimuli is caused by gradual loss of MAPK-dependent protection in Drosophila.Aging cell · 2022Article
- Regulation of Phosphorylated State of NMDA Receptor by STEPAntioxidants (Basel, Switzerland) · 2021Article
- STEP inhibition prevents Aβ-mediated damage in dendritic complexity and spine density in Alzheimer's disease.Experimental brain research · 2021Article
- Insight into the Role of the STriatal-Enriched Protein Tyrosine Phosphatase (STEP) in AFrontiers in pharmacology · 2021Article
- Regulation of glutamate receptors by striatal-enriched tyrosine phosphatase 61 (STEPThe Journal of physiology · 2021Review
- The Implication of STEP in Synaptic Plasticity and Cognitive Impairments in Alzheimer's Disease and Other Neurological Disorders.Frontiers in cell and developmental biology · 2021Review
- Rislenemdaz treatment in the lateral habenula improves despair-like behavior in mice.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2020Article
- Alterations of STEP46 and STEP61 Expression in the Rat Retina with Age and AMD-Like Retinopathy Development.International journal of molecular sciences · 2020Article
- Neuroligin-1 is altered in the hippocampus of Alzheimer's disease patients and mouse models, and modulates the toxicity of amyloid-beta oligomers.Scientific reports · 2020Article
- Proteolytic Degradation of Hippocampal STEPMolecular neurobiology · 2019Article
- Effects of estrogen and aging on synaptic morphology and distribution of phosphorylated Tyr1472 NR2B in the female rat hippocampus.Neurobiology of aging · 2019Article
- Social Memory and Social Patterns Alterations in the Absence of STriatal-Enriched Protein Tyrosine Phosphatase.Frontiers in behavioral neuroscience · 2018Article
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Authors and funding
15 authors at 8 institutions in 3 countries.
Funding
Abstract
Cognitive disabilities that occur with age represent a growing and expensive health problem. Age-associated memory deficits are observed across many species, but the underlying molecular mechanisms remain to be fully identified. Here, we report elevations in the levels and activity of the striatal-enriched phosphatase (STEP) in the hippocampus of aged memory-impaired mice and rats, in aged rhesus monkeys, and in people diagnosed with amnestic mild cognitive impairment (aMCI). The accumulation of STEP with aging is related to dysfunction of the ubiquitin-proteasome system that normally leads to the degradation of STEP. Higher level of active STEP is linked to enhanced dephosphorylation of its substrates GluN2B and ERK1/2, CREB inactivation, and a decrease in total levels of GluN2B and brain-derived neurotrophic factor (BDNF). These molecular events are reversed in aged STEP knockout and heterozygous mice, which perform similarly to young control mice in the Morris water maze (MWM) and Y-maze tasks. In addition, administration of the STEP inhibitor TC-2153 to old rats significantly improved performance in a delayed alternation T-maze memory task. In contrast, viral-mediated STEP overexpression in the hippocampus is sufficient to induce memory impairment in the MWM and Y-maze tests, and these cognitive deficits are reversed by STEP inhibition. In old LOU/C/Jall rats, a model of healthy aging with preserved memory capacities, levels of STEP and GluN2B are stable, and phosphorylation of GluN2B and ERK1/2 is unaltered. Altogether, these data suggest that elevated levels of STEP that appear with advancing age in several species contribute to the cognitive declines associated with aging.
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Registered trials
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