English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Evaluation of: Lim Y, Kehm VM, Lee EB et al. α-syn suppression reverses synaptic and memory defects in a mouse model of dementia with Lewy bodies. J. Neurosci. 31, 10076–10087 (2011). This study reports on the regional and time-dependent pathological changes of mice expressing human wild-type or A53T-mutant α-synuclein under the control of a CaMKIIα promoter as well as a tetracycline-regulated transactivator. The transgene was turned on from postnatal day 21 onwards. A53T-mutant α-synuclein expression leads to a dementia with Lewy body-like phenotype. A presynaptic α-synuclein-related pathology goes hand-in-hand with memory impairment as measured by conditioned fear. By turning off the α-synuclein transgene at a particular time point after a synaptic pathology has already been developed, a regression of the α-synuclein-related changes can be observed and the memory impairment does not progress or even mildly improves.

future neurology

A transgenic mouse model of dementia with Lewy bodies suggests a link between α-synuclein expression, presynaptic vesicle pathology and cognitive deficit