Identification of gene networks mediating regional resistance to tauopathy in late-onset Alzheimer's disease.
Christopher A AyoubConnor S WagnerJeff KuretPublished in: PLoS genetics (2023)
Neurofibrillary lesions composed of tau protein aggregates are defining hallmarks of Alzheimer's Disease. Despite tau filaments appearing to spread between networked brain regions in a prion-like manner, certain areas including cerebellum resist trans-synaptic spread of tauopathy and degeneration of their constituent neuronal cell bodies. To identify molecular correlates of resistance, we derived and implemented a ratio of ratios approach for disaggregating gene expression data on the basis of regional vulnerability to tauopathic neurodegeneration. When applied to vulnerable pre-frontal cortex as an internal reference for resistant cerebellum, the approach segregated adaptive changes in expression into two components. The first was enriched for neuron-derived transcripts associated with proteostasis including specific members of the molecular chaperone family and was unique to resistant cerebellum. When produced as purified proteins, each of the identified chaperones depressed aggregation of 2N4R tau in vitro at sub-stoichiometric concentrations, consistent with the expression polarity deduced from ratio of ratios testing. In contrast, the second component enriched for glia- and microglia-derived transcripts associated with neuroinflammation, segregating these pathways from susceptibility to tauopathy. These data support the utility of ratio of ratios testing for establishing the polarity of gene expression changes with respect to selective vulnerability. The approach has the potential to identify new targets for drug discovery predicated on their ability to promote resistance to disease in vulnerable neuron populations.
Keyphrases
- gene expression
- late onset
- poor prognosis
- drug discovery
- cerebrospinal fluid
- electronic health record
- dna methylation
- functional connectivity
- early onset
- cerebral ischemia
- resting state
- cognitive decline
- magnetic resonance
- binding protein
- inflammatory response
- genome wide
- single cell
- magnetic resonance imaging
- traumatic brain injury
- mesenchymal stem cells
- spinal cord
- risk assessment
- oxidative stress
- cognitive impairment
- lps induced
- bone marrow
- neuropathic pain
- heat shock
- copy number
- stem cells
- big data
- protein protein
- small molecule
- computed tomography
- contrast enhanced
- transcription factor