Synaptic tau: A pathological or physiological phenomenon? DOI Creative Commons
Miranda Robbins, Emma L. Clayton, Gabriele S. Kaminski Schierle

и другие.

Acta Neuropathologica Communications, Год журнала: 2021, Номер 9(1)

Опубликована: Сен. 9, 2021

Abstract In this review, we discuss the synaptic aspects of Tau pathology occurring during Alzheimer’s disease (AD) and how may relate to memory impairment, a major hallmark AD. Whilst clinical diagnosis AD patients is loss working long-term declarative memory, histological presence neurofibrillary tangles hyperphosphorylated Amyloid-beta plaques. spreads through synaptically connected neurons impair function preceding formation tangles, loss, axonal retraction cell death. Alongside pathology, recent data suggest that has physiological roles in pre- or post- compartments. Thus, have seen shift research focus from as microtubule-stabilising protein axons, with accelerating spine formation, dendritic elongation, plasticity coordinating pathways. We collate here myriad emerging interactions Tau, current evidence contributes

Язык: Английский

The effect of insomnia on development of Alzheimer’s disease DOI Creative Commons
Shaghayegh Sadeghmousavi,

Mahsa Eskian,

Farzaneh Rahmani

и другие.

Journal of Neuroinflammation, Год журнала: 2020, Номер 17(1)

Опубликована: Окт. 6, 2020

Abstract Alzheimer’s disease (AD) is the most common type of dementia and a neurodegenerative disorder characterized by memory deficits especially forgetting recent information, recall ability impairment, loss time tracking, problem-solving, language, recognition difficulties. AD also globally important health issue but despite all scientific efforts, treatment still challenge. Sleep has roles in learning consolidation. Studies have shown that sleep deprivation (SD) insomnia are associated with pathogenesis may an impact on symptoms development. Thus, disorders decisive effects AD; this association deserves more attention research, diagnostics, treatment, knowing relation can help to prevent through screening proper management disorders. This study aimed show potential role SD progression AD.

Язык: Английский

Процитировано

80

Possible Mechanisms of Tau Spread and Toxicity in Alzheimer’s Disease DOI Creative Commons
Huiqin Zhang, Yu Cao, Lina Ma

и другие.

Frontiers in Cell and Developmental Biology, Год журнала: 2021, Номер 9

Опубликована: Июль 28, 2021

Tau is a protein that associates with microtubules (MTs) and promotes their assembly stability. The loses its ability to bind MTs in tauopathies, detached tau can misfold induce the pathological changes characterize Alzheimer’s disease (AD). A growing body of evidence indicates tauopathies spread between cells or connected regions. Pathological transmission brain patients AD other due various species along neuroanatomically regions “prion-like” manner. This complex process involves multiple steps secretion, cellular uptake, transcellular transfer, and/or seeding, but precise mechanisms pathology propagation remain unclear. review summarizes current on nature propagative possible involved spread, including detachment from MTs, degradations, discusses different underlying pathology.

Язык: Английский

Процитировано

78

Therapeutic Potential of Vital Transcription Factors in Alzheimer’s and Parkinson’s Disease With Particular Emphasis on Transcription Factor EB Mediated Autophagy DOI Creative Commons
Sachchida Nand, Neeraj Tiwari, Payal Singh

и другие.

Frontiers in Neuroscience, Год журнала: 2021, Номер 15

Опубликована: Дек. 14, 2021

Autophagy is an important cellular self-digestion and recycling pathway that helps in maintaining homeostasis. Dysregulation at various steps of the autophagic endolysosomal has been reported several neurodegenerative disorders such as Alzheimer’s disease (AD), Parkinson’s (PD), Huntington (HD) cited a critically feature for central nervous system (CNS) proteostasis. Recently, another molecular target, namely transcription factor EB (TFEB) explored globally to treat disorders. This TFEB, key regulator autophagy lysosomal biogenesis pathway. Multiple research studies suggested therapeutic potential by targeting TFEB human diseases involving autophagy-lysosomal dysfunction, especially A common observation all their poor efficacy clearing recycle toxic aggregated proteins damaged organelles due impairment dysfunction characterized accumulation protein aggregates leads progressive loss structural integrity/functionality neurons may even result neuronal death. In recent years biogenesis, received considerable attention. It emerged target numerous like AD PD. neurobiology animal models, found ameliorate neurotoxicity rescue neurodegeneration. Since master transcriptional plays crucial role defining activation. Studies have done understand mechanisms which yield insights into how might be targeted used strategy develop treatment process with extensive application this review, we explore different factor-based therapy some natural compounds PD special emphasis on TFEB.

Язык: Английский

Процитировано

74

Promiscuous Roles of Autophagy and Proteasome in Neurodegenerative Proteinopathies DOI Open Access
Fiona Limanaqi, Francesca Biagioni, Stefano Gambardella

и другие.

International Journal of Molecular Sciences, Год журнала: 2020, Номер 21(8), С. 3028 - 3028

Опубликована: Апрель 24, 2020

Alterations in autophagy and the ubiquitin proteasome system (UPS) are commonly implicated protein aggregation toxicity which manifest a number of neurological disorders. In fact, both UPS alterations bound to aggregation, spreading so-called prionoid proteins, including alpha synuclein (α-syn), amyloid-beta (Aβ), tau, huntingtin, superoxide dismutase-1 (SOD-1), TAR-DNA-binding 43 kDa (TDP-43) fused sarcoma (FUS). Recent biochemical morphological studies add this scenario, focusing on coordinated, either synergistic or compensatory, interplay that occurs between UPS. pathways such as mammalian target rapamycin (mTOR), transcription factor EB (TFEB), Bcl2-associated athanogene 1/3 (BAG3/1) glycogen synthase kinase beta (GSk3β), widely explored potential targets neurodegenerative proteinopathies, operate at crossroad These steps key orchestrating specificity magnitude two degradation systems for effective homeostasis, while intermingling with intracellular secretory/trafficking inflammatory pathways. The findings discussed present manuscript supposed novel viewpoints may further enrich our insight complex interactions occurring cell-clearing systems, misfolding propagation. Discovering mechanisms enabling cross-talk is expected provide molecular proteinopathies.

Язык: Английский

Процитировано

72

Synaptic tau: A pathological or physiological phenomenon? DOI Creative Commons
Miranda Robbins, Emma L. Clayton, Gabriele S. Kaminski Schierle

и другие.

Acta Neuropathologica Communications, Год журнала: 2021, Номер 9(1)

Опубликована: Сен. 9, 2021

Abstract In this review, we discuss the synaptic aspects of Tau pathology occurring during Alzheimer’s disease (AD) and how may relate to memory impairment, a major hallmark AD. Whilst clinical diagnosis AD patients is loss working long-term declarative memory, histological presence neurofibrillary tangles hyperphosphorylated Amyloid-beta plaques. spreads through synaptically connected neurons impair function preceding formation tangles, loss, axonal retraction cell death. Alongside pathology, recent data suggest that has physiological roles in pre- or post- compartments. Thus, have seen shift research focus from as microtubule-stabilising protein axons, with accelerating spine formation, dendritic elongation, plasticity coordinating pathways. We collate here myriad emerging interactions Tau, current evidence contributes

Язык: Английский

Процитировано

70