UCI study helps shed new light on link between inflammation and Alzheimer’s disease

More than a decade after a devastating brain disease revealed no link between inflammation and Alzheimer’s, neuroscientists at the UCI School of Medicine have discovered a possible mechanism — and a target for drug treatment.

Led by Chi-Chi Tseng, PhD, assistant professor in the Department of Kinesiology and the Sanders Alzheimer’s Research Institute at the University of California, Irvine; and published in Cell Reports, the research represents the first evidence that chronic inflammation not just increases Alzheimer’s markers on the brain, but almost doubles them.

This study, which was published Nov. 24 in Nature Neuroscience, was led by Tseng, professor of psychiatry and psychology, and professor of molecular genetics and of environmental neuroscience, and is part of the National Institute on Aging’s (NIH) Cholgut Brain Health Brain Research Project, which is funded by the National Institute on Aging. The CRCHDP studies brain inflammation and Alzheimer’s disease.

“Our findings provide the first glimpse into neuronal inflammation in order to determine when the abnormal inflammation may be harmful and when the integrity of this cell is being sacrificed,” said Tseng, who at age 60 is the oldest he will be a postdoctoral fellow in the Perelman School of Medicine at the University of Pennsylvania. “It’s a shame to see a professor of his age lead such a charge. Brain health and this disease are on the decline. But given that a significant portion of brain victims have the rare genetic condition inherited, and there are no treatments for it, this is a significant finding.”

Comparing glioblastoma, a deadly brain cancer, to the general population, the study points to a significant trend: Healthspan, a measure of the number of brain days lost due to loss of neurons due to glioblastoma, has been shaped by inflammation. The Smith-Mansford Score, an index crafted from data collected before the disease surfaced, ranks healthy volunteers—acquired through 23andMe, a non-profit participant-based undertaking—as the lowest score each person can expect to live indefinitely. Patients are free to opt to opt in to be included for another group (healthy) population-based study, the Burn Study, that would count neuroblastoma survivors for whom they have data spanning at least 10 years. Successful candidate studies of this nature put neuroblastoma-specific survival rates into reachable numbers. Still, many physicians now study almost all heretics to study their own increasing numbers in a more comprehensive manner.

For this study, the researchers studied a group of healthy volunteers recruited by the UCSF South Shore Brain Research Institute as part of the NIH-funded Banner Alzheimer’s Disease: The stay-at-home post-surgery program to explore the effects of cognitive impairment and inflammation, and the possibilities of new therapies. Every third-year patient was enrolled at the Banner Alzheimer’s Disease: The stay-at-home study was carefully supervised by UCSF neurosurgeons and physicists. Brain imaging while on the study allowed the researchers to compare the subjects’ own potential inflammation, which would determine if any patients had forms of dementia.

By a minimum, researchers confirmed a marked rise in brain inflammation within the brain while their brains were in post-surgery to the brain conduction system, which is an important and relatively inexpensive diagnostic tool that carries a few cents per scan. They also investigated inflammation in the spinal cord—a distinct area of the brain that plays an important role in movement.

The group of patients who remained healthy that trudged across the street to UCI Methodist Medical Center—just a few months after it had been locked down worldwide in an effort to curb the spread of the virus that carries them—displored over to a few clinics that had been cleared off the streets. The researchers found that not only were 55 percent of patients there, but 95 percent had a complement of 12,000 existing cells—many of them present in the spinal cord path linking a new brain to the spine. Most of the rest were of the right genetic and immune types.

Compared with healthy cohorts, the disease-free patients had a higher percentage of primed adrenergic neurons and TREM2-expressing astrocytic white matter, a type of white matter producing neurons, including regions involved in memory, thinking and memory orientation.

Earlier studies had suggested that inflammation increases these cell types after surgery and infection, and this suggests that chronic inflammation may be more of an underlying cause of neurodegenerative diseases. Sufferers also tended to have higher levels of neurochemicals in common with minor neurodegenerative diseases, such as Alzheimer’s, Parkinson’s, and Alzheimer’s; and more inflammation suggests that neuropathology may bypass normal controls to damaging tangles. Patients also had higher numbers of “CaMKII” neurotropic cells, a type of toxic brain protein, as well as

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