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Farris, C.

Publications and source records attributed to Farris, C..

2 recordsLinked to original sources

Amyloidosis and tauopathy progressively disrupt near-critical dynamics in selectively vulnerable circuits

Mechanistically distinct neurodegenerative diseases result in similar cognitive deficits, and pathology is often concentrated in a set of circuits known to be selectively vulnerable. Selective vulnerability is an intrinsic property of a circuit: in APP/PS1 mice, where plaques are global, functional disruptions are confined to circuits within the default mode network. What characterizes the dynamics of vulnerable circuits from those of spared circuits is unknown. We asked whether the distinguishing property is the proximity of population dynamics to criticality, a homeostatic set-point of network activity that determines computational capacity. We recorded single units simultaneously in three selectively vulnerable regions (retrosplenial cortex, anterior cingulate cortex, and CA1 hippocampus) and in primary visual cortex of freely behaving young and old APP/PS1 and wild-type mice. Firing rate and spike-time variability differed by genotype inconsistently across regions and ages. In contrast, three measures from criticality theory each revealed deficits that emerged only with age and only in the vulnerable regions. No measure detected a progressive change in V1. Avalanche scaling is not fixed in neural activity, but varies along a scaling line as the network state changes. As a result, the lines generated by each genotype revealed a constitutive effect of the transgene in young animals, which inverted with age in amyloid-bearing animals, but only in vulnerable circuits. If the destabilization of near-critical dynamics directly reflects a circuit's functional capacity, the same signature should identify a mechanistically distinct degenerative disease. In a model of tauopathy (P301S/E4), CA1 dynamics were displaced from the control scaling line with the same age-dependent reversal observed in APP/PS1. Our results suggest a network-level principle of neurodegenerative diseases: molecularly unrelated pathologies converge on the loss of near-critical dynamics in selectively vulnerable circuits.

neuroscience↗

Circuit-specific selective vulnerability in the DMN persists in the face of widespread amyloid burden.

The relationship between brainwide functional decline and accumulation of pathological protein aggregates in Alzheimers disease (AD) is complex and not well understood. A set of highly interconnected cortical regions known as the default mode network (DMN) exhibits selective vulnerability to both functional decline and amyloid beta (A{beta}) plaques in early AD. One possibility is that early A{beta} accumulation in the DMN drives vulnerability. However, it is unknown whether there is something intrinsic to neuronal projections within the DMN that biases these circuits towards dysfunction. Here we directly test this hypothesis using long-term recordings of the spiking activity of ensembles of single units in freely behaving mice characterized by global cortical and hippocampal A{beta} burden (APP/PS1). Specifically, we track the interactions of a population of neurons within a DMN region and two additional populations that comprise monosynaptic targets, one within and the other outside the DMN. In addition, we record single neurons in hippocampus and examine interactions between the in-DMN and out-DMN cortical circuits triggered on hippocampal sharp-wave ripples, stereotyped hippocampal events that contribute to memory consolidation in the cortex. We examine the statistics of local activity as well as inter-regional communication in a region, genotype, and brain-state dependent manner. Our data reveal dysfunction restricted to the in-DMN projecting circuit. In contrast, communication along neuronal projections that originate in the DMN but target an out-DMN population is equivalent in APP/PS1 and WT mice. Circuit dysfunction is most evident throughout sleep, and particularly disrupted within sharp-wave ripples. Summarily, our results indicate that, even in the face of transgene overexpression and widespread A{beta}, there is distinct intrinsic and selective vulnerability. This vulnerability to amyloidosis is circuit-specific and conditioned on target, and neither source nor amyloid burden. These data raise the possibility that neuronal function in the DMN is not universally vulnerable; DMN subnetworks whose interactions involve targets outside the DMN may be resilient to A{beta}.

neuroscience↗