Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Cognitive deficits in Tsc1+/- mice in the absence of cerebral lesions and seizures.

Annals of neurology - 1 Dec 2007

Goorden Susanna M I, van Woerden Geeske M, van der Weerd Louise, Cheadle Jeremy P, Elgersma Ype

Abstract excerpt

OBJECTIVE: Tuberous sclerosis complex (TSC) is characterized by brain lesions, epilepsy, increased incidence of mental retardation and autism. The causal link between lesion load and epilepsy on cognitive disabilities has been debated, and these factors explain only part of the intelligence quotient variability. A Tsc2 rat model of the disease provided evidence that the TSC genes are directly involved in neuronal...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Conditioning, Psychological
Share to Dendrites

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Maze Learning

Share to Nesting Behavior

Share to Seizures

Share to Social Behavior

Share to Tuberous Sclerosis Complex 1 Protein

Source

Identifiers

PMID: 18067135
DOI: 10.1002/ana.21317

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Cognitive deficits in Tsc1+/- mice in the absence of cerebral lesions and seizures.PMID 18067135Read ↗

A Mouse Model of Tuberous Sclerosis: Neuronal Loss of Tsc1 Causes Dysplastic and Ectopic Neurons, Reduced Myelination, Seizure Activity, and Limited SurvivalSemantic proximity Read ↗

A circuitry and biochemical basis for tuberous sclerosis symptoms: from epilepsy to neurocognitive deficitsSemantic proximity Read ↗

From mTOR to cognition: molecular and cellular mechanisms of cognitive impairments in tuberous sclerosisSemantic proximity Read ↗

Tsc2 gene inactivation causes a more severe epilepsy phenotype than Tsc1 inactivation in a mouse model of tuberous sclerosis complex.Semantic proximity Read ↗

Increased levels of anxiety-related behaviors in a Tsc2 dominant negative transgenic mouse model of tuberous sclerosis.Semantic proximity Read ↗

Mechanisms of neurocognitive dysfunction and therapeutic considerations in tuberous sclerosis complexSemantic proximity Read ↗

Revisiting Brain Tuberous Sclerosis Complex in Rat and Human: Shared Molecular and Cellular Pathology Leads to Distinct Neurophysiological and Behavioral Phenotypes.Semantic proximity Read ↗

Single-cell Tsc1 knockout during corticogenesis generates tuber-like lesions and reduces seizure threshold in miceSemantic proximity Read ↗

Graded loss of tuberin in an allelic series of brain models of TSC correlates with survival, and biochemical, histological and behavioral features.Semantic proximity Read ↗

Reversal of learning deficits in a Tsc2+/− mouse model of tuberous sclerosisSemantic proximity Read ↗

Tuberous sclerosis complex and epilepsy: recent developments and future challenges.Semantic proximity Read ↗

Tsc2 mutation rather than Tsc1 mutation dominantly causes a social deficit in a mouse model of tuberous sclerosis complex.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.