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Article
Open AccessOutside-in signaling through the major histocompatibility complex class-I cytoplasmic tail modulates glutamate receptor expression in neurons
The interplay between AMPA-type glutamate receptors (AMPARs) and major histocompatibility complex class I (MHC-I) proteins in regulating synaptic signaling is a crucial aspect of central nervous system (CNS) f...
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Article
Open AccessThe intracellular domain of major histocompatibility class-I proteins is essential for maintaining excitatory spine density and synaptic ultrastructure in the brain
Major histocompatibility complex class I (MHC-I) proteins are expressed in neurons, where they regulate synaptic plasticity. However, the mechanisms by which MHC-I functions in the CNS remains unknown. Here we...
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Article
Open AccessGalactic cosmic radiation exposure causes multifaceted neurocognitive impairments
Technological advancements have facilitated the implementation of realistic, terrestrial-based complex 33-beam galactic cosmic radiation simulations (GCR Sim) to now probe central nervous system functionality....
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Open AccessBrain and blood biomarkers of tauopathy and neuronal injury in humans and rats with neurobehavioral syndromes following blast exposure
Traumatic brain injury (TBI) is a risk factor for the later development of neurodegenerative diseases that may have various underlying pathologies. Chronic traumatic encephalopathy (CTE) in particular is assoc...
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Open AccessLaterality and region-specific tau phosphorylation correlate with PTSD-related behavioral traits in rats exposed to repetitive low-level blast
Military veterans who experience blast-related traumatic brain injuries often suffer from chronic cognitive and neurobehavioral syndromes. Reports of abnormal tau processing following blast injury have raised ...
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Article
Open AccessAltered synaptic ultrastructure in the prefrontal cortex of Shank3-deficient rats
Deletion or mutations of SHANK3 lead to Phelan–McDermid syndrome and monogenic forms of autism spectrum disorder (ASD). SHANK3 encodes its eponymous scaffolding protein at excitatory glutamatergic synapses. Alter...
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Article
Open AccessChronic Exposure to High Altitude: Synaptic, Astroglial and Memory Changes
Long-term operations carried out at high altitude (HA) by military personnel, pilots, and astronauts may trigger health complications. In particular, chronic exposure to high altitude (CEHA) has been associate...
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Article
Cell- and layer-specific transcriptomic strategy for characterizing the molecular phenotype of rat cortical neurons using laser capture microdissection and massively parallel RNA sequencing
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Open AccessAdolescent exposure to Δ9-tetrahydrocannabinol alters the transcriptional trajectory and dendritic architecture of prefrontal pyramidal neurons
Neuronal circuits within the prefrontal cortex (PFC) mediate higher cognitive functions and emotional regulation that are disrupted in psychiatric disorders. The PFC undergoes significant maturation during ado...
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Autism spectrum disorder: neuropathology and animal models
Autism spectrum disorder (ASD) has a major impact on the development and social integration of affected individuals and is the most heritable of psychiatric disorders. An increase in the incidence of ASD cases...
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Article
Open AccessMajor Histocompatibility Complex class I proteins are critical for maintaining neuronal structural complexity in the aging brain
Major histocompatibility complex class I (MHCI) proteins have been implicated in neuronal function through the modulation of neuritogenesis, synaptogenesis, synaptic plasticity and memory consolidation during ...
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Article
Open AccessPhysiologically generated presenilin 1 lacking exon 8 fails to rescue brain PS1−/− phenotype and forms complexes with wildtype PS1 and nicastrin
The presenilin 1 (PSEN1) L271V mutation causes early-onset familial Alzheimer’s disease by disrupting the alternative splicing of the PSEN1 gene, producing some transcripts harboring the L271V point mutation and ...
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Article
Open AccessUltrastructural analyses in the hippocampus CA1 field in Shank3-deficient mice
The genetics of autism spectrum disorder (hereafter referred to as “autism”) are rapidly unfolding, with a significant increase in the identification of genes implicated in the disorder. Many of these genes ar...
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Article
Open AccessAltered synaptic structure in the hippocampus in a mouse model of Alzheimer’s disease with soluble amyloid-β oligomers and no plaque pathology
Mounting evidence suggests that soluble oligomers of amyloid-β (oAβ) represent the pertinent synaptotoxic form of Aβ in sporadic Alzheimer’s disease (AD); however, the mechanistic links between oAβ and synapti...
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Article
Open AccessSelective vulnerability of the cerebral vasculature to blast injury in a rat model of mild traumatic brain injury
Blast-related traumatic brain injury (TBI) is a common cause of injury in the military operations in Iraq and Afghanistan. How the primary blast wave affects the brain is not well understood. The aim of the pr...
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Article
Adjusting the compass: new insights into the role of angiogenesis in Alzheimer’s disease
Growing evidence suggests that vascular perturbation plays a critical role in the pathogenesis of Alzheimer’s disease (AD). It appears to be a common feature in addition to the classic pathological hallmarks o...
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Open AccessBlast overpressure induces shear-related injuries in the brain of rats exposed to a mild traumatic brain injury
Blast-related traumatic brain injury (TBI) has been a significant cause of injury in the military operations of Iraq and Afghanistan, affecting as many as 10-20% of returning veterans. However, how blast waves...
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Article
Region-specific neuron and synapse loss in the hippocampus of APPSL/PS1 knock-in mice
Transgenic mouse models with knock-in (KI) expression of human mutant amyloid precursor protein (APP) and/or human presenilin 1 (PS1) may be helpful to elucidate the cellular consequences of APP and PS1 mispro...
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Article
Open AccessCessation of Neoangiogenesis in Alzheimer's Disease Follows Amyloid-beta Immunization
Pathogenic neoangiogenesis in Alzheimer's disease (AD) is due to amyloid-beta (Aβ) and results in blood-brain barrier (BBB) leakiness in AD. It likely occurs as a compensatory response to impaired cerebral blo...
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Open AccessThe isotropic fractionator provides evidence for differential loss of hippocampal neurons in two mouse models of Alzheimer's disease
The accumulation of amyloid beta (Aβ) oligomers or fibrils is thought to be one of the main causes of synaptic and neuron loss, believed to underlie cognitive dysfunction in Alzheimer’s disease (AD). Neuron lo...
