Christy Y. Hung

Tat Chee Ave
Kowloon, KKC, Hong Kong Special Administrative Region

Last Updated: 09/26/2026

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Found 14 publications

A tanycytic route for tau clearance in Alzheimer's disease.

A tanycytic route for tau clearance in Alzheimer's disease.

Journal: Trends in neurosciences

Published: March 20, 2026

Tau uptake by human neurons depends on receptor LRP1 and kinase LRRK2.

Tau uptake by human neurons depends on receptor LRP1 and kinase LRRK2.

Journal: The EMBO journal

Published: January 27, 2025

Mislocalization of nucleic acids is a convergent and targetable mechanism in Alzheimer's disease and frontotemporal dementia.

Mislocalization of nucleic acids is a convergent and targetable mechanism in Alzheimer's disease and frontotemporal dementia.

Journal: Cell reports

Published: December 10, 2024

APP antisense oligonucleotides are effective in rescuing mitochondrial phenotypes in human iPSC-derived trisomy 21 astrocytes.

APP antisense oligonucleotides are effective in rescuing mitochondrial phenotypes in human iPSC-derived trisomy 21 astrocytes.

Journal: Alzheimer's & dementia : the journal of the Alzheimer's Association

Published: September 04, 2024

Clearance of beta-amyloid and tau aggregates is size dependent and altered by an inflammatory challenge.

Clearance of beta-amyloid and tau aggregates is size dependent and altered by an inflammatory challenge.

Journal: Brain communications

Published: July 06, 2024

Therapeutic potential of APP antisense oligonucleotides for Alzheimer's disease and down syndrome-related Alzheimer's disease.

Therapeutic potential of APP antisense oligonucleotides for Alzheimer's disease and down syndrome-related Alzheimer's disease.

Journal: Molecular neurodegeneration

Published: May 14, 2024

4R tau drives endolysosomal and autophagy dysfunction in frontotemporal dementia.

4R tau drives endolysosomal and autophagy dysfunction in frontotemporal dementia.

Journal: Autophagy

Published: January 04, 2024

APP antisense oligonucleotides reduce amyloid-β aggregation and rescue endolysosomal dysfunction in Alzheimer's disease.

APP antisense oligonucleotides reduce amyloid-β aggregation and rescue endolysosomal dysfunction in Alzheimer's disease.

Journal: Brain : a journal of neurology

Published: September 11, 2023

Elevated 4R tau contributes to endolysosomal dysfunction and neurodegeneration in VCP-related frontotemporal dementia.

Elevated 4R tau contributes to endolysosomal dysfunction and neurodegeneration in VCP-related frontotemporal dementia.

Journal: Brain : a journal of neurology

Published: April 11, 2023

Endolysosome and autophagy dysfunction in Alzheimer disease.

Endolysosome and autophagy dysfunction in Alzheimer disease.

Journal: Autophagy

Published: August 25, 2021

SORL1 deficiency in human excitatory neurons causes APP-dependent defects in the endolysosome-autophagy network.

SORL1 deficiency in human excitatory neurons causes APP-dependent defects in the endolysosome-autophagy network.

Journal: Cell reports

Published: April 08, 2020

Altered γ-Secretase Processing of APP Disrupts Lysosome and Autophagosome Function in Monogenic Alzheimer's Disease.

Altered γ-Secretase Processing of APP Disrupts Lysosome and Autophagosome Function in Monogenic Alzheimer's Disease.

Journal: Cell reports

Published: August 07, 2018

Showing 1-12 of 14

Last Updated: 09/26/2026