Reelin, tau phosphorylation and psychiatric complications in patients with hippocampal sclerosis and structural abnormalities in temporal lobe epilepsy

Machado, René Andrade; Benjumea-Cuartas, Vanesa; Berruecos, José Fernando Zapata; Agudelo-Flóres, Piedad Matilde; Salazar-Peláez, Lina María

doi:10.1016/j.yebeh.2019.04.052

Cited by 20 publications

(15 citation statements)

References 58 publications

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“…Encompassing more than 80 phosphorylation sites targeted by more than 30 kinases (Sergeant et al , 2008), tau could be viewed as a homeostatic protein, like A 2A R, which can be modulated in detrimental situations. In line, previous work reported tau hyperphosphorylation in conditions eliciting A 2A R synaptic upregulation such as stress or epilepsy (Lopes et al , 2016; Machado et al , 2019). Therefore, the sole increase of A 2A R alone is not sufficient to promote tau hyperphosphorylation.…”

Section: Discussionsupporting

confidence: 91%

Exacerbation of C1q dysregulation, synaptic loss and memory deficits in tau pathology linked to neuronal adenosine A2A receptor

Carvalho

Faivre

Pietrowski

et al. 2019

Brain

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See Cunha (doi:10.1093/brain/awz335) for a scientific commentary on this article. Carvalho et al. provide clues to the onset of immune dysregulation underlying early synaptic loss in Alzheimer’s disease and tauopathies, by linking overactivation of adenosine A2A receptors in tau pathology to a particular microglial signature (upregulation of C1q and TREM2) allied to the loss of glutamatergic synapses and cognitive deficits.

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Section: Discussionsupporting

confidence: 91%

Exacerbation of C1q dysregulation, synaptic loss and memory deficits in tau pathology linked to neuronal adenosine A2A receptor

Carvalho

Faivre

Pietrowski

et al. 2019

Brain

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“…The phosphorylated Dab1 prevents tau phosphorylation. In advanced AD, Aβ increases reelin levels and further disrupts active homodimers [ 45 , 47 - 49 ]. Thus, increased reelin observed in NFL players at risk of CTE may suggest increase in tau phosphorylation due to altered reelin signaling.…”

Section: Discussionmentioning

confidence: 99%

Proteomic Profiling of Extracellular Vesicles Separated from Plasma of Former National Football League Players at Risk for Chronic Traumatic Encephalopathy

et al. 2021

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Chronic Traumatic Encephalopathy (CTE) is a tauopathy that affects individuals with a history of exposure to repetitive head impacts, including National Football League (NFL) players. Extracellular vesicles (EVs) are known to carry tau in Alzheimer's disease and other tauopathies. We examined protein profiles of EVs separated from the plasma of former NFL players at risk for CTE. EVs were separated from the plasma from former NFL players and age-matched controls using size-exclusion chromatography. Label-free quantitative proteomic analysis identified 675 proteins in plasma EVs, and 17 proteins were significantly differentially expressed between former NFL players and controls. Total tau (t-tau) and tau phosphorylated at threonie181 (p-tau181) in plasma-derived EVs were measured by ultrasensitive immunoassay. Level of t-tau and p-tau181 in EVs were significantly different, and the area under the receiver operating characteristic curve (AUC) of t-tau and p-tau181 showed 0.736 and 0.715, respectively. Machine learning analysis indicated that a combination of collagen type VI alpha 3 and 1 chain (COL6A3 and COL6A1) and reelin (RELN) can distinguish former NFL players from controls with 85% accuracy (AUC = 0.85). Based on the plasma EV proteomics, these data provide protein profiling of plasma EVs for CTE, and indicate combination of COL6A3, RELN and COL6A1 in plasma EVs may serve as the potential diagnostic biomarkers for CTE.

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“…As mentioned earlier, many other mechanisms have been suggested, such as the APO-ε4 allele, ( 97 – 99 ), and an early reduction in the level of either the mitochondrial protein deacetylase sirtuin 3 ( 100 ) or reelin [( 101 , 102 ), reviewed by ( 103 )].…”

Section: Potential Mechanistic Underpinnings Of Ad-related Neuronal H...mentioning

confidence: 99%

Sleep: The Tip of the Iceberg in the Bidirectional Link Between Alzheimer's Disease and Epilepsy

et al. 2022

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The observation that a pathophysiological link might exist between Alzheimer's disease (AD) and epilepsy dates back to the identification of the first cases of the pathology itself and is now strongly supported by an ever-increasing mountain of literature. An overwhelming majority of data suggests not only a higher prevalence of epilepsy in Alzheimer's disease compared to healthy aging, but also that AD patients with a comorbid epileptic syndrome, even subclinical, have a steeper cognitive decline. Moreover, clinical and preclinical investigations have revealed a marked sleep-related increase in the frequency of epileptic activities. This characteristic might provide clues to the pathophysiological pathways underlying this comorbidity. Furthermore, the preferential sleep-related occurrence of epileptic events opens up the possibility that they might hasten cognitive decline by interfering with the delicately orchestrated synchrony of oscillatory activities implicated in sleep-related memory consolidation. Therefore, we scrutinized the literature for mechanisms that might promote sleep-related epileptic activity in AD and, possibly dementia onset in epilepsy, and we also aimed to determine to what degree and through which processes such events might alter the progression of AD. Finally, we discuss the implications for patient care and try to identify a common basis for methodological considerations for future research and clinical practice.

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Reelin, tau phosphorylation and psychiatric complications in patients with hippocampal sclerosis and structural abnormalities in temporal lobe epilepsy

Cited by 20 publications

References 58 publications

Exacerbation of C1q dysregulation, synaptic loss and memory deficits in tau pathology linked to neuronal adenosine A2A receptor

Exacerbation of C1q dysregulation, synaptic loss and memory deficits in tau pathology linked to neuronal adenosine A2A receptor

Proteomic Profiling of Extracellular Vesicles Separated from Plasma of Former National Football League Players at Risk for Chronic Traumatic Encephalopathy

Sleep: The Tip of the Iceberg in the Bidirectional Link Between Alzheimer's Disease and Epilepsy

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