Four-repeat tauopathies DOI

Thomas W. Rösler,

Amir Tayaranian Marvian, Matthias Brendel

и другие.

Progress in Neurobiology, Год журнала: 2019, Номер 180, С. 101644 - 101644

Опубликована: Июнь 22, 2019

Язык: Английский

Sleep Loss Can Cause Death through Accumulation of Reactive Oxygen Species in the Gut DOI Creative Commons
Alexandra Vaccaro,

Yosef Kaplan Dor,

Keishi Nambara

и другие.

Cell, Год журнала: 2020, Номер 181(6), С. 1307 - 1328.e15

Опубликована: Июнь 1, 2020

Язык: Английский

Процитировано

387

Association Between Sleep Duration and Cognitive Decline DOI Creative Commons
Yanjun Ma, Lirong Liang, Fanfan Zheng

и другие.

JAMA Network Open, Год журнала: 2020, Номер 3(9), С. e2013573 - e2013573

Опубликована: Сен. 21, 2020

An association between sleep duration and the trajectory of cognitive decline has not been conclusively demonstrated.

Язык: Английский

Процитировано

353

Fluid transport in the brain DOI
Martin Kaag Rasmussen, Humberto Mestre, Maiken Nedergaard

и другие.

Physiological Reviews, Год журнала: 2021, Номер 102(2), С. 1025 - 1151

Опубликована: Май 5, 2021

The brain harbors a unique ability to, figuratively speaking, shift its gears. During wakefulness, the is geared fully toward processing information and behaving, while homeostatic functions predominate during sleep. blood-brain barrier establishes stable environment that optimal for neuronal function, yet imposes physiological problem; transcapillary filtration forms extracellular fluid in other organs reduced to minimum brain. Consequently, depends on special [the cerebrospinal (CSF)] flushed into along perivascular spaces created by astrocytic vascular endfeet. We describe this pathway, coined term glymphatic system, based dependency endfeet their adluminal expression of aquaporin-4 water channels facing CSF-filled spaces. Glymphatic clearance potentially harmful metabolic or protein waste products, such as amyloid-β, primarily active sleep, when drivers, cardiac cycle, respiration, slow vasomotion, together efficiently propel CSF inflow periarterial brain's space contains an abundance proteoglycans hyaluronan, which provide low-resistance hydraulic conduit rapidly can expand shrink sleep-wake cycle. system brain, meets requisites maintain homeostasis similar peripheral organs, considering blood-brain-barrier paths formation egress CSF.

Язык: Английский

Процитировано

344

The different autophagy degradation pathways and neurodegeneration DOI Creative Commons
Angeleen Fleming, Mathieu Bourdenx,

Motoki Fujimaki

и другие.

Neuron, Год журнала: 2022, Номер 110(6), С. 935 - 966

Опубликована: Фев. 7, 2022

Язык: Английский

Процитировано

308

Obstructive sleep apnea, cognition and Alzheimer's disease: A systematic review integrating three decades of multidisciplinary research DOI
Omonigho Michael Bubu,

Andreia G. Andrade,

Ogie Queen Umasabor‐Bubu

и другие.

Sleep Medicine Reviews, Год журнала: 2019, Номер 50, С. 101250 - 101250

Опубликована: Дек. 12, 2019

Язык: Английский

Процитировано

275

Mechanisms of secretion and spreading of pathological tau protein DOI Creative Commons
Cecilia A. Brunello,

Maria Merezhko,

Riikka‐Liisa Uronen

и другие.

Cellular and Molecular Life Sciences, Год журнала: 2019, Номер 77(9), С. 1721 - 1744

Опубликована: Окт. 30, 2019

Abstract Accumulation of misfolded and aggregated forms tau protein in the brain is a neuropathological hallmark tauopathies, such as Alzheimer’s disease frontotemporal lobar degeneration. Tau aggregates have ability to transfer from one cell another induce templated misfolding aggregation healthy molecules previously cells, thereby propagating pathology across different areas prion-like manner. The molecular mechanisms involved cell-to-cell are diverse, not mutually exclusive only partially understood. Intracellular accumulation induces several that aim reduce cellular burden proteins also promote secretion aggregates. However, may be released cells physiologically unrelated aggregation. involves multiple vesicular non-vesicle-mediated pathways, including directly through plasma membrane. Consequently, extracellular can found various forms, both free vesicles, exosomes ectosomes. Once space, internalized by neighboring neurons glial via endocytic, pinocytic phagocytic mechanisms. Importantly, accumulating evidence suggests propagation could provide general mechanism for progression tauopathies other related neurodegenerative diseases. Here, we review recent literature on tau, with particular focus secretion.

Язык: Английский

Процитировано

255

Microglia, Lifestyle Stress, and Neurodegeneration DOI Creative Commons
Charlotte Madore, Zhuoran Yin, Jeffrey Leibowitz

и другие.

Immunity, Год журнала: 2020, Номер 52(2), С. 222 - 240

Опубликована: Янв. 7, 2020

Язык: Английский

Процитировано

254

Sleep deprivation impairs molecular clearance from the human brain DOI Open Access
Per Kristian Eide, Vegard Vinje, Are Hugo Pripp

и другие.

Brain, Год журнала: 2020, Номер 144(3), С. 863 - 874

Опубликована: Дек. 5, 2020

It remains an enigma why human beings spend one-third of their life asleep. Experimental data suggest that sleep is required for clearance waste products from brain metabolism. This has, however, never been verified in humans. The primary aim the present study was to examine vivo whether one night total deprivation affects molecular brain. Secondarily, we examined affected by subsequent sleep. Multiphase MRI with standardized T1 sequences performed up 48 h after intrathecal administration contrast agent gadobutrol (0.5 ml 1 mmol/ml), which served as a tracer molecule. Using FreeSurfer software, quantified enrichment within 85 regions percentage change baseline normalized signals. cerebral compared between two cohorts individuals; cohort (n = 7) underwent Day 2 (sleep group) while age and gender-matched control group 17; allowed free 2. From 3 all individuals were enriched brains groups similarly. Sleep sole intervention. One impaired substance most regions, including cortex, white matter limbic structures, demonstrated on morning intervention deprivation/sleep). Moreover, not compensated 3. results provide evidence impairs brain, humans do catch lost

Язык: Английский

Процитировано

251

Modifiable Risk Factors for Alzheimer’s Disease DOI Creative Commons
George A. Edwards, Nazaret Gamez, Gabriel Escobedo

и другие.

Frontiers in Aging Neuroscience, Год журнала: 2019, Номер 11

Опубликована: Июнь 24, 2019

Since first described in the early 1900s, Alzheimer's disease (AD) has risen exponentially prevalence and concern. Research still drives to understand etiology pathogenesis of this what risk factors can attribute AD. With a majority AD cases being sporadic origin, increasing exponential growth an aged population lack treatment, it is imperative discover easy accessible preventative method for Some increase propensity such as aging, sex, genetics. Moreover, there are also modifiable factors-in terms treatable medical conditions lifestyle choices-that play role developing These have their own biological mechanisms that may contribute pathological consequences. In review article, we will discuss current literature how each these interplay into development progression if strategically analyzed treated, could aid protection against neurodegenerative disease.

Язык: Английский

Процитировано

224

Sleep deprivation and its association with diseases- a review DOI
Siaw-Cheok Liew, Thida Aung

Sleep Medicine, Год журнала: 2020, Номер 77, С. 192 - 204

Опубликована: Авг. 18, 2020

Язык: Английский

Процитировано

209