Tau secretion and propagation: Perspectives for potential preventive interventions in Alzheimer's disease and other tauopathies

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F61989592%3A15110%2F21%3A73607380" target="_blank" >RIV/61989592:15110/21:73607380 - isvavai.cz</a>

Výsledek na webu

<a href="https://www.sciencedirect.com/science/article/pii/S001448862100162X?via%3Dihub" target="_blank" >https://www.sciencedirect.com/science/article/pii/S001448862100162X?via%3Dihub</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1016/j.expneurol.2021.113756" target="_blank" >10.1016/j.expneurol.2021.113756</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Tau secretion and propagation: Perspectives for potential preventive interventions in Alzheimer's disease and other tauopathies

Popis výsledku v původním jazyce

Alzheimer&apos;s disease (AD) is characterised by the accumulation of intracytoplasmic aggregates of tau protein, which are suggested to spread in a prion-like manner between interconnected brain regions. This spreading is mediated by the secretion and uptake of tau from the extracellular space or direct cell-to-cell transmission through cellular protrusions. The prion-like tau then converts the endogenous, normal tau into pathological forms, resulting in neurodegeneration. The endoplasmic reticulum/Golgi-independent tau secretion through unconventional secretory pathways involves delivering misfolded and aggregated tau to the plasma membrane and its release into the extracellular space by non-vesicular and vesicular mechanisms. Although cytoplasmic tau was thought to be released only from degenerating cells, studies now show that cells constitutively secrete tau at low levels under physiological conditions. The mechanisms of secretion of tau under physiological and pathological conditions remain unclear. Therefore, a better understanding of these pathways is essential for developing therapeutic approaches that can target prion-like tau forms to prevent neurodegeneration progression in AD. This review focuses on unconventional secretion pathways involved in the spread of tau pathology in AD and presents these pathways as prospective areas for future AD drug discovery and development.

Název v anglickém jazyce

Tau secretion and propagation: Perspectives for potential preventive interventions in Alzheimer's disease and other tauopathies

Popis výsledku anglicky

Alzheimer&apos;s disease (AD) is characterised by the accumulation of intracytoplasmic aggregates of tau protein, which are suggested to spread in a prion-like manner between interconnected brain regions. This spreading is mediated by the secretion and uptake of tau from the extracellular space or direct cell-to-cell transmission through cellular protrusions. The prion-like tau then converts the endogenous, normal tau into pathological forms, resulting in neurodegeneration. The endoplasmic reticulum/Golgi-independent tau secretion through unconventional secretory pathways involves delivering misfolded and aggregated tau to the plasma membrane and its release into the extracellular space by non-vesicular and vesicular mechanisms. Although cytoplasmic tau was thought to be released only from degenerating cells, studies now show that cells constitutively secrete tau at low levels under physiological conditions. The mechanisms of secretion of tau under physiological and pathological conditions remain unclear. Therefore, a better understanding of these pathways is essential for developing therapeutic approaches that can target prion-like tau forms to prevent neurodegeneration progression in AD. This review focuses on unconventional secretion pathways involved in the spread of tau pathology in AD and presents these pathways as prospective areas for future AD drug discovery and development.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

10608 - Biochemistry and molecular biology

Projekt

Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Rok uplatnění

2021

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

EXPERIMENTAL NEUROLOGY

ISSN

0014-4886

e-ISSN

—

Svazek periodika

343

Číslo periodika v rámci svazku

113756

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

13

Strana od-do

"nestránkováno"

Kód UT WoS článku

000679110400005

EID výsledku v databázi Scopus

2-s2.0-85106605913