ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013
PAK inactivation impairs social recognition in 3xTg-AD Mice without increasing brain deposition of tau and Aβ.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 40 citations in OpenAlex.
- PAK1 inhibitor NVS-PAK1-1 preserves dendritic spines in amyloid/tau exposed neurons and 5xFAD mice.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Differential impact of eicosapentaenoic acid and docosahexaenoic acid in an animal model of Alzheimer's disease.Journal of lipid research · 2024Article
- Postsynaptic Protein Shank3a Deficiency Synergizes with Alzheimer's Disease Neuropathology to Impair Cognitive Performance in the 3xTg-AD Murine Model.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Article
- The molecular basis of p21-activated kinase-associated neurodevelopmental disorders: From genotype to phenotype.Frontiers in neuroscience · 2023Review
- Insights into early pathogenesis of sporadic Alzheimer's disease: role of oxidative stress and loss of synaptic proteins.Frontiers in neuroscience · 2023Article
- Investigation of Anxiety- and Depressive-like Symptoms in 4- and 8-Month-Old Male Triple Transgenic Mouse Models of Alzheimer's Disease.International journal of molecular sciences · 2022Article
- Artificial intelligence framework identifies candidate targets for drug repurposing in Alzheimer's disease.Alzheimer's research & therapy · 2022Article
- The p21-activated kinases in neural cytoskeletal remodeling and related neurological disorders.Protein & cell · 2022Review
- Role of Retinoid X Receptors (RXRs) and dietary vitamin A in Alzheimer's disease: Evidence from clinicopathological and preclinical studies.Neurobiology of disease · 2021Article
- Differential effects of chronic immunosuppression on behavioral, epigenetic, and Alzheimer's disease-associated markers in 3xTg-AD mice.Alzheimer's research & therapy · 2021Article
- Tetrahydrobiopterin Improves Recognition Memory in the Triple-Transgenic Mouse Model of Alzheimer's Disease, Without Altering Amyloid-β and Tau Pathologies.Journal of Alzheimer's disease : JAD · 2021Article
- Sex-dependent alterations in the physiology of entorhinal cortex neurons in old heterozygous 3xTg-AD mice.Biology of sex differences · 2020Article
- Stress gates an astrocytic energy reservoir to impair synaptic plasticity.Nature communications · 2020Article
- Synaptic actin stabilization protein loss in Down syndrome and Alzheimer disease.Brain pathology (Zurich, Switzerland) · 2020Article
- The Role of ADF/Cofilin in Synaptic Physiology and Alzheimer's Disease.Frontiers in cell and developmental biology · 2020Review
- Cofilin, a Master Node Regulating Cytoskeletal Pathogenesis in Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2019Review
- Impaired AMPA signaling and cytoskeletal alterations induce early synaptic dysfunction in a mouse model of Alzheimer's disease.Aging cell · 2018Article
- Religious Orders Study and Rush Memory and Aging Project.Journal of Alzheimer's disease : JAD · 2018Review
- A modified formulation of Huanglian-Jie-Du-Tang reduces memory impairments and β-amyloid plaques in a triple transgenic mouse model of Alzheimer's disease.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
Defects in p21-activated kinase (PAK) are suspected to play a role in cognitive symptoms of Alzheimer's disease (AD). Dysfunction in PAK leads to cofilin activation, drebrin displacement from its actin-binding site, actin depolymerization/severing, and, ultimately, defects in spine dynamics and cognitive impairment in mice. To determine the role of PAK in AD, we first quantified PAK by immunoblotting in homogenates from the parietal neocortex of subjects with a clinical diagnosis of no cognitive impairment (n = 12), mild cognitive impairment (n = 12), or AD (n = 12). A loss of total PAK, detected in the cortex of AD patients (-39% versus controls), was correlated with cognitive impairment (r(2) = 0.148, p = 0.027) and deposition of total and phosphorylated tau (r(2) = 0.235 and r(2) = 0.206, respectively), but not with Aβ42 (r(2) = 0.056). Accordingly, we found a decrease of total PAK in the cortex of 12- and 20-month-old 3xTg-AD mice, an animal model of AD-like Aβ and tau neuropathologies. To determine whether PAK dysfunction aggravates AD phenotype, 3xTg-AD mice were crossed with dominant-negative PAK mice. PAK inactivation led to obliteration of social recognition in old 3xTg-AD mice, which was associated with a decrease in cortical drebrin (-25%), but without enhancement of Aβ/tau pathology or any clear electrophysiological signature. Overall, our data suggest that PAK decrease is a consequence of AD neuropathology and that therapeutic activation of PAK may exert symptomatic benefits on high brain function.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.