TREM2 signalling as a multifaceted player in brain homoeostasis and a potential target for Alzheimer's disease treatment

Ayyubova, Gunel

doi:10.1111/ejn.15914

Cited by 10 publications

(4 citation statements)

References 110 publications

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“…Interactions exclusive to opNSCs were apolipoprotein E (APOE) from mural cells and macrophage/microglia, and clusterin (CLU) from ependymal cells, interacting with the Triggering Receptor Expressed on Myeloid cells 2 (TREM2), implicating opNSCs in response to injury, neuroprotection, and degenerative pathologies ( 73, 74 ).…”

Section: Resultsmentioning

confidence: 99%

Identity and Nature of Neural Stem Cells in the Adult Human Subventricular Zone

Baig,

Nadaf,

Allache

et al. 2023

Preprint

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The existence of neural stem cells (NSCs) in adult human brain neurogenic regions remains unresolved. To address this, we created a cell atlas of the adult human subventricular zone (SVZ) derived from fresh neurosurgical samples using single-cell transcriptomics. We discovered 2 adult radial glia (RG)-like populations, aRG1 and aRG2. aRG1 shared features with fetal early RG (eRG) and aRG2 were transcriptomically similar to fetal outer RG (oRG). We also captured early neuronal and oligodendrocytic NSC states. We found that the biological programs driven by their transcriptomes support their roles as early-lineage NSCs. Finally, we show that these NSCs have the potential to transition between states and along lineage trajectories. These data reveal that multipotent NSCs reside in the adult human SVZ.

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Section: Resultsmentioning

confidence: 99%

Identity and Nature of Neural Stem Cells in the Adult Human Subventricular Zone

Baig,

Nadaf,

Allache

et al. 2023

Preprint

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“…Testing this same group with CD68 lysosomal immunoglobin, a lower activity was shown in the sleep-deprived group. Hence, Trem2-dependent microglia were in a less functioning state after sleep deprivation [14].…”

Section: Sleep Deprivation Impacts Trem2 Expressing In Microgliamentioning

confidence: 99%

TREM2 mediated A clearance dysfunction in microglia cells by circadian disruption in Alzheimer's disease

2023

TNS

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Genome-wide association studies (GWAS) have shown that the Trem2 gene is a risk factor associated with the onset of Alzheimer's Disease (AD). The Trem2 gene is highly expressed on the surface membrane of microglia cells in the central neuron system (CNS), which mediates neuron inflammation and the clearance of axons and synapses. As a growing amount of evidence is connecting Circadian disruptions with increased levels of CNS inflammation, this review aims to find a connection between circadian disruption and amyloid-leading Alzheimers disease through Trem2 in Microglia cells. This review summarizes past research independently about the circadian disruption with microglia activation, microglia activation with Trem2, and Trem2-affected MG cells impacting the development of Alzheimers Disease. Further research may focus on specifying the importance of Trem2 microglia cells caused neuron inflammation in the development of Alzheimer's pathology, for whether the early A-beta plaquing is triggered by Trem2 microglia cells, or Trem2 is just contributing but not the causation of AD in its Mild Cognitive impairment (MCI) stage.

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“…The microglial receptors CD33 and TREM2 modulate microglial pathology and neuroinflammation. TREM2 variants like p. R47H reduce the Aβ phagocytic ability of microglia and increase the risk of AD by two to four times, disrupting the microglial function and reducing the progression of the disease [63]. On the other hand, CD33 opposes the effects of TREM2 signaling and acts as the microglial phagocytosis negative regulator downstream of TREM2 [64].…”

Section: Neuroinflammation In Alzheimer's Diseasementioning

confidence: 99%

Biomarkers in Alzheimer’s Disease: Are Olfactory Neuronal Precursors Useful for Antemortem Biomarker Research?

Santillán-Morales,

Rodriguez-Espinosa,

Muñoz-Estrada

et al. 2024

Brain Sciences

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Alzheimer’s disease (AD), as the main cause of dementia, affects millions of people around the world, whose diagnosis is based mainly on clinical criteria. Unfortunately, the diagnosis is obtained very late, when the neurodegenerative damage is significant for most patients. Therefore, the exhaustive study of biomarkers is indispensable for diagnostic, prognostic, and even follow-up support. AD is a multifactorial disease, and knowing its underlying pathological mechanisms is crucial to propose new and valuable biomarkers. In this review, we summarize some of the main biomarkers described in AD, which have been evaluated mainly by imaging studies in cerebrospinal fluid and blood samples. Furthermore, we describe and propose neuronal precursors derived from the olfactory neuroepithelium as a potential resource to evaluate some of the widely known biomarkers of AD and to gear toward searching for new biomarkers. These neuronal lineage cells, which can be obtained directly from patients through a non-invasive and outpatient procedure, display several characteristics that validate them as a surrogate model to study the central nervous system, allowing the analysis of AD pathophysiological processes. Moreover, the ease of obtaining and harvesting endows them as an accessible and powerful resource to evaluate biomarkers in clinical practice.

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TREM2 signalling as a multifaceted player in brain homoeostasis and a potential target for Alzheimer's disease treatment

Cited by 10 publications

References 110 publications

Identity and Nature of Neural Stem Cells in the Adult Human Subventricular Zone

Identity and Nature of Neural Stem Cells in the Adult Human Subventricular Zone

TREM2 mediated A clearance dysfunction in microglia cells by circadian disruption in Alzheimer's disease

Biomarkers in Alzheimer’s Disease: Are Olfactory Neuronal Precursors Useful for Antemortem Biomarker Research?

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