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

Tau is required for progressive synaptic and memory deficits in a transgenic mouse model of α-synucleinopathy

6 Jun 2019

Abstract excerpt

Parkinson’s disease dementia (PDD) and dementia with Lewy bodies (DLB) are clinically and neuropathologically highly related α-synucleinopathies that collectively constitute the second leading cause of neurodegenerative dementias. Genetic and neuropathological studies directly implicate α-synuclein (αS) abnormalities in PDD and DLB pathogenesis. However, it is currently unknown how αS abnormalities contribute to...

Read the complete abstract on PubMed

Topics

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

Share to Alzheimer's disease research and treatments
Share to Nerve injury and regeneration
Share to Parkinson's Disease Mechanisms and Treatments

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 31168644
DOI: 10.1007/s00401-019-02032-w

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Tau is required for progressive synaptic and memory deficits in a transgenic mouse model of α-synucleinopathyPMID 31168644Read ↗

Loss of Tau Expression Attenuates Neurodegeneration Associated With α-SynucleinopathySemantic proximity Read ↗

Behavioral characterization of A53T mice reveals early and late stage deficits related to Parkinson's disease.Semantic proximity Read ↗

Tau knockout exacerbates degeneration of parvalbumin-positive neurons in substantia nigra pars reticulata in Parkinson's disease-related α-synuclein A53T mice.Semantic proximity Read ↗

Reducing tau ameliorates behavioural and transcriptional deficits in a novel model of Alzheimer’s diseaseSemantic proximity Read ↗

Acute tau knockdown in the hippocampus of adult mice causes learning and memory deficitsSemantic proximity Read ↗

Motor deficits and brain pathology in the Parkinson’s disease mouse model hA53TtgSemantic proximity Read ↗

Mouse models of alpha-synucleinopathy and Lewy pathology.Semantic proximity Read ↗

Age-dependent effects of A53T alpha-synuclein on behavior and dopaminergic function.Semantic proximity Read ↗

α-Syn suppression reverses synaptic and memory defects in a mouse model of dementia with Lewy bodies.Semantic proximity Read ↗

Neuropathology in mice expressing human alpha-synuclein.Semantic proximity Read ↗

Neuropathology in Mice Expressing Human α-SynucleinSemantic proximity Read ↗

A role for tau in learning, memory and synaptic plasticitySemantic proximity Read ↗

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