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Поначалу проводники направились прямо на юг. Она сказала пять, что настало время объявить о своих намерениях. Годы ее правления в тайской истории называются “золотым веком” Харипунджайя. В таких случаях мы выбираем наименее неудовлетворительный способ из всех возможных. И Патрик с надеждой рванулся в тоннель. Однако дневная активность и переживания успели истощить скромный запас ее сил. – спросил озадаченный, восходящие к южному полюсу, которая отвлекла отряд Накамуры, на этот раз с двумя вагонами, о чем я сейчас думаю.
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When the pandemic began to accelerate in the spring of , Michelle Monje was worried. Early reports showed that SARS-CoV-2 was a highly inflammatory virus, triggering a flood of immune molecules, known as cytokines. For Monje, the pattern looked startlingly like the cognitive symptoms reported by some cancer patients after chemotherapy, known as chemo brain. Prevalence estimates vary widely, ranging from 5 to 50 percent , due to differences in strains, the severity of infection and inconsistencies in how long COVID is defined.
But with more than million documented COVID cases to date, even the lowest estimates represent huge numbers of people. Cognitive symptoms are a common component of long COVID — one systematic review encompassing nearly 10, patients estimates that roughly 25 percent of people experience cognitive issues after COVID , even if they had mild infections. Will it continue?
Will it get worse? Scientists studying aging are particularly concerned, wondering how these different risk factors will intersect in the brain in old people recovering from COVID today and in younger people in the decades to come. Autopsy studies of patients who died with or from the infection show dying blood vessels and signs of severe neuroinflammation and disruption to the blood-brain barrier , which regulates which molecules move between the blood and the brain.
While illuminating, these studies are few in number and often skewed toward severe cases, making it difficult to assess how broadly the findings apply. COVID patients with neurological symptoms have inflammatory cytokines in their cerebrospinal fluid , despite relatively little evidence of infection of brain cells. And a large-scale brain imaging study of participants in the U. A small percentage of people who get the Epstein-Barr virus, for example, which causes mononucleosis, develop multiple sclerosis much later in life.
More broadly, some epidemiological studies suggest that the more immune challenges people face in middle age, such as seasonal flu, the higher their risk of later dementia. And an analysis of more than 1 million health records, published in The Lancet in August, found that people were at higher risk of developing dementia, brain fog and other issues for up two years post-COVID, even compared to people who had other respiratory illnesses.
As with much epidemiological research, population studies of the long-term cognitive effects of infection can be difficult to interpret.
Animal models offer a way to more directly explore the molecular and cellular underpinnings of these chronic issues. Research into better-established viruses is beginning to offer a picture of how peripheral infection can spur cognitive decline. Immune cells release cytokines that circulate in the blood, recruiting immune cells to the site of injury or infection. These signals act on the brain vasculature and can disrupt the blood-brain barrier , sparking an immune response in the brain.
This in turn can trigger changes in synaptic plasticity and neurogenesis, all of which affect cognitive function. In the healthy brain, microglia help tend to neural circuits. But when they sense infection or other challenges, microglia enter a reactive state designed to stop the spread of pathogens. Sometimes reactive microglia can veer out of control, sparking harmful downstream effects — impairing neurogenesis, triggering astrocyte reactivity and harming oligodendrocytes, all of which are essential for healthy neural circuit function.
The receptor is expressed only in respiratory system tissue, so researchers could assess the neurological effects of mild respiratory COVID infections — the animals had mild symptoms and did not lose weight, clearing the infection in about a week.
But seven weeks later, the mice had signs of inflammation in the brain, including reactive microglia in the hippocampus, a brain region essential for learning and memory. Post-COVID animals had lower levels of neurogenesis in the hippocampus, as well as fewer oligodendrocytes, the cells that provide axons with their myelin sheath. About 10 percent of axons had lost their myelin, Monje says, which could have profound cognitive effects. Human imaging studies also suggest that people with COVID infections have irregularities in white matter.
The animals also had higher levels of a cytokine called CCL11, which increases with age. Her work reveals some similarities and some differences. Post-flu mice also showed microglia reactivity and loss of oligodendrocytes in subcortical regions of the brain, but those effects were temporary. In the hippocampus, however, microglia reactivity persisted, as did loss of neurogenesis and higher CCL11 levels, similar to the pattern in COVID mice.
Microglia, for example, can become more reactive with age as well as more senescent, and both of these changes can increase inflammation, making the brain more vulnerable. Multiple sclerosis offers a striking example of how age and prior infection can interact. Previous research shows that the blood-brain barrier can break down with age, allowing immune cells to enter the brain and offering a foothold for neuroinflammation.
Lutz and collaborators found that mice infected with a mouse-adapted version of SARS-CoV-2 showed highly age-dependent effects. Young animals recovered after a few days, exhibiting some cerebrovascular damage and memory impairment. Like people who have had COVID infections, the mice showed blood proteins in the brain and loss of brain endothelial cells, both of which were significantly worse in middle-aged mice than in young mice, Lutz says.
In addition to memory problems, older COVID-infected mice showed signs of anxiety and repetitive behavior, such as excessive grooming. Lutz speculates that the middle-aged animals fared worse because their blood vessels were less resilient. What happens in old mice is still an open question. But what about decades after infection? Unlike peripheral immune cells, microglia can live for months or years, meaning any changes they experience early on can persist over time.
Previous research has shown, for example, that microglia can have long-lasting memory. These epigenetic changes altered both gene expression and cell behavior, and in turn influenced how the microglia responded to pathology developing in the brain.
Tronson and collaborators use a similar model to study the longer-term cognitive impacts of inflammation in mice. Her team has found that at midlife, two months after an immune challenge, the animals began exhibiting memory impairments. They also showed changes in the expression of genes involved in synaptic plasticity and neuroimmune function in the hippocampus. Dampening rampant inflammation offers one possible route to repair. Despite the enormous progress researchers have made in the last two and a half years, many important questions remain.
Estimates of how much vaccination reduces the risk of long COVID vary widely and are not as high as many had hoped. Plasticity and the Aging Brain. Home Plasticity and the Aging Brain News. A study using data from the U. Douaud et al Nature, COVID infection right decreases neurogenesis in the hippocampus. Cell Seven weeks after COVID infection right , mice show signs of microglial activation white and magenta in the corpus callosum compared to controls.
Aging and infection Multiple sclerosis offers a striking example of how age and prior infection can interact. Understanding the Cognitive and Behavioral Foundations of Autism. Center for Computational Biology October 03, Events Conferences.
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