Decoupling of Global Brain Activity and Cerebrospinal Fluid Flow in Parkinson's Disease Cognitive Decline

2021 ◽  
Author(s):  
Feng Han ◽  
Gregory L. Brown ◽  
Yalin Zhu ◽  
Aaron E. Belkin‐Rosen ◽  
Mechelle M. Lewis ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Cerebrospinal Fluid ◽  
Fluid Flow ◽  
Cognitive Decline ◽  
Brain Activity ◽  
Cerebrospinal Fluid Flow ◽  
Global Brain

Differentiating progressive supranuclear palsy from Parkinson's disease by MRI-based dynamic cerebrospinal fluid flow

2015 ◽  
Vol 357 (1-2) ◽  
pp. 178-182 ◽  
Author(s):  
Yusuke Fukui ◽  
Nozomi Hishikawa ◽  
Kota Sato ◽  
Taijun Yunoki ◽  
Syoichiro Kono ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Cerebrospinal Fluid ◽  
Fluid Flow ◽  
Progressive Supranuclear Palsy ◽  
Cerebrospinal Fluid Flow

Ratios of proteins in cerebrospinal fluid in Parkinson's disease cognitive decline: prospective study

2018 ◽  
Vol 33 (11) ◽  
pp. 1809-1813 ◽  
Author(s):  
Manuel Delgado-Alvarado ◽  
Rosalía Dacosta-Aguayo ◽  
Irene Navalpotro-Gómez ◽  
Belén Gago ◽  
Ana Gorostidi ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Cerebrospinal Fluid ◽  
Prospective Study ◽  
Cognitive Decline

Cognitive decline in Parkinson's disease is associated with slowing of resting-state brain activity: a longitudinal study

2013 ◽  
Vol 34 (2) ◽  
pp. 408-418 ◽  
Author(s):  
Kim T.E. Olde Dubbelink ◽  
Diederick Stoffers ◽  
Jan Berend Deijen ◽  
Jos W.R. Twisk ◽  
Cornelis J. Stam ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Longitudinal Study ◽  
Cognitive Decline ◽  
Resting State ◽  
Brain Activity

scholarly journals Cerebrospinal fluid N-224 tau helps discriminate Alzheimer’s disease from subjective cognitive decline and other dementias

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Claudia Cicognola ◽  
Oskar Hansson ◽  
Philip Scheltens ◽  
Hlin Kvartsberg ◽  
Henrik Zetterberg ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Parkinson’S Disease ◽  
Alzheimer's Disease ◽  
Parkinson's Disease ◽  
Cerebrospinal Fluid ◽  
Cognitive Decline ◽  
Subjective Cognitive Decline ◽  
Study Cohort ◽  
Not Otherwise Specified ◽  
T Tau

Abstract Background Elevated cerebrospinal fluid (CSF) concentrations of total tau (T-tau) and phosphorylated tau at Thr181 (P-tau181) protein are typical of Alzheimer’s disease (AD). However, the T-tau assay measures only the mid-region of the protein, while tau in CSF is instead composed of a series of fragments. One fragment species in particular, N-224, shows increased levels in AD compared to controls. In this multicentre study, we performed a clinical validation of the N-224 assay in cohorts including patients with subjective cognitive decline (SCD), mild cognitive impairment (MCI), AD, non-AD dementias and controls. Methods Cohorts consisted of 30 SCD and 30 probable AD from the Amsterdam Dementia Cohort (cohort 1) and 539 controls, 195 SCD, 232 MCI, 137 AD and 253 non-AD from the Swedish BioFINDER study (cohort 2). All samples had AD core biomarkers (Aβ42, T-tau, P-tau181) measurements. N-224 was measured with an in-house ultrasensitive Simoa assay. Results N-224 levels were significantly higher in AD compared to SCD (cohort 1: p = 0.003) and in AD compared to all other diagnostic groups in cohort 2 (control, SCD, MCI and non-AD, p < 0.0001). Within the non-AD group, N-224 showed significantly lower concentrations compared to AD in Parkinson’s disease (PD, p < 0.0001), Parkinson’s disease dementia (PDD, p = 0.004), progressive supranuclear palsy (PSP, < 0.0001), multiple system atrophy (MSA, p = 0.002) and parkinsonisms not otherwise specified (NOS, p = 0.007). In cohort 1, higher concentrations of N-224 were associated to lower Mini-Mental State Examination (MMSE) scores (R2 = 0.318, β = 0.564, p ≤ 0.0001) and could accurately identify a pathological (< 24) MMSE score (p < 0.0001, AUC = 0.824). Conclusions N-224 tau can distinguish AD subjects from SCD and can discriminate subgroups of non-AD dementias from AD. Therefore, N-224 may be a useful addition to the tau biomarker toolbox for the study of tau species in CSF and for better understanding disease pathogenesis.

scholarly journals Reduced coupling between cerebrospinal fluid flow and global brain activity is linked to Alzheimer disease–related pathology

PLoS Biology ◽  
2021 ◽  
Vol 19 (6) ◽  
pp. e3001233
Author(s):  
Feng Han ◽  
Jing Chen ◽  
Aaron Belkin-Rosen ◽  
Yameng Gu ◽  
Liying Luo ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Alzheimer Disease ◽  
Driving Forces ◽  
Brain Activity ◽  
Amyloid Β ◽  
High Amplitude ◽  
Tau Proteins ◽  
Cerebrospinal Fluid Flow ◽  
Metabolite Clearance ◽  
Global Brain

The glymphatic system plays an important role in clearing the amyloid-β (Aβ) and tau proteins that are closely linked to Alzheimer disease (AD) pathology. Glymphatic clearance, as well as Aβ accumulation, is highly dependent on sleep, but the sleep-dependent driving forces behind cerebrospinal fluid (CSF) movements essential to the glymphatic flux remain largely unclear. Recent studies have reported that widespread, high-amplitude spontaneous brain activations in the drowsy state and during sleep, which are shown as large global signal peaks in resting-state functional magnetic resonance imaging (rsfMRI), are coupled with CSF movements, suggesting their potential link to glymphatic flux and metabolite clearance. By analyzing multimodal data from the Alzheimer’s Disease Neuroimaging Initiative (ADNI) project, here we showed that the coupling between the global fMRI signal and CSF influx is correlated with AD-related pathology, including various risk factors for AD, the severity of AD-related diseases, the cortical Aβ level, and cognitive decline over a 2-year follow-up. These results provide critical initial evidence for involvement of sleep-dependent global brain activity, as well as the associated physiological modulations, in the clearance of AD-related brain waste.

scholarly journals Biomarkers of neurodegeneration and glial activation validated in Alzheimer’s disease assessed in longitudinal cerebrospinal fluid samples of Parkinson’s disease

PLoS ONE ◽  
2021 ◽  
Vol 16 (10) ◽  
pp. e0257372
Author(s):  
Michael Bartl ◽  
Mohammed Dakna ◽  
Douglas Galasko ◽  
Samantha J. Hutten ◽  
Tatiana Foroud ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Parkinson’S Disease ◽  
Alzheimer's Disease ◽  
Parkinson's Disease ◽  
Cerebrospinal Fluid ◽  
Cognitive Decline ◽  
Neurofilament Light Chain ◽  
Significant Difference

Aim Several pathophysiological processes are involved in Parkinson’s disease (PD) and could inform in vivo biomarkers. We assessed an established biomarker panel, validated in Alzheimer’s Disease, in a PD cohort. Methods Longitudinal cerebrospinal fluid (CSF) samples from PPMI (252 PD, 115 healthy controls, HC) were analyzed at six timepoints (baseline, 6, 12, 24, 36, and 48 months follow-up) using Elecsys® electrochemiluminescence immunoassays to quantify neurofilament light chain (NfL), soluble TREM2 receptor (sTREM2), chitinase-3-like protein 1 (YKL40), glial fibrillary acidic protein (GFAP), interleukin-6 (IL-6), S100, and total α-synuclein (αSyn). Results αSyn was significantly lower in PD (mean 103 pg/ml vs. HC: 127 pg/ml, p<0.01; area under the curve [AUC]: 0.64), while all other biomarkers were not significantly different (AUC NfL: 0.49, sTREM2: 0.54, YKL40: 0.57, GFAP: 0.55, IL-6: 0.53, S100: 0.54, p>0.05) and none showed a significant difference longitudinally. We found significantly higher levels of all these markers between PD patients who developed cognitive decline during follow-up, except for αSyn and IL-6. Conclusion Except for αSyn, the additional biomarkers did not differentiate PD and HC, and none showed longitudinal differences, but most markers predict cognitive decline in PD during follow-up.

Intraoperative localization of spatially and spectrally distinct resting-state networks in Parkinson’s disease

2020 ◽  
Vol 132 (4) ◽  
pp. 1234-1242 ◽  
Author(s):  
Paolo Belardinelli ◽  
Ramin Azodi-Avval ◽  
Erick Ortiz ◽  
Georgios Naros ◽  
Florian Grimm ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Network Effects ◽  
Brain Activity ◽  
Dynamic Imaging ◽  
Oscillatory Activity ◽  
Network Information ◽  
Novel Approach ◽  
Electrophysiological Recordings ◽  
Intraoperative Localization

Deep brain stimulation (DBS) of the subthalamic nucleus (STN) is an effective treatment for symptomatic Parkinson’s disease (PD); the clinical benefit may not only mirror modulation of local STN activity but also reflect consecutive network effects on cortical oscillatory activity. Moreover, STN-DBS selectively suppresses spatially and spectrally distinct patterns of synchronous oscillatory activity within cortical-subcortical loops. These STN-cortical circuits have been described in PD patients using magnetoencephalography after surgery. This network information, however, is currently not available during surgery to inform the implantation strategy.The authors recorded spontaneous brain activity in 3 awake patients with PD (mean age 67 ± 14 years; mean disease duration 13 ± 7 years) during implantation of DBS electrodes into the STN after overnight withdrawal of dopaminergic medication. Intraoperative propofol was discontinued at least 30 minutes prior to the electrophysiological recordings. The authors used a novel approach for performing simultaneous recordings of STN local field potentials (LFPs) and multichannel electroencephalography (EEG) at rest. Coherent oscillations between LFP and EEG sensors were computed, and subsequent dynamic imaging of coherent sources was performed.The authors identified coherent activity in the upper beta range (21–35 Hz) between the STN and the ipsilateral mesial (pre)motor area. Coherence in the theta range (4–6 Hz) was detected in the ipsilateral prefrontal area.These findings demonstrate the feasibility of detecting frequency-specific and spatially distinct synchronization between the STN and cortex during DBS surgery. Mapping the STN with this technique may disentangle different functional loops relevant for refined targeting during DBS implantation.

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