Age-Related Decrease in Tyrosine Hydroxylase Immunoreactivity in the Substantia Nigra and Region-Specific Changes in Microglia Morphology in HIV-1 Tg Rats

Dr, Goulding; Kraft, Andrew D.; Pr, Mouton; Ca, McPherson; Avdoshina,; Mocchetti, Italo; Gj, Harry

doi:10.1007/s12640-019-00077-z

Cited by 5 publications

(4 citation statements)

References 97 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The increased and chronic inflammatory status in the brain may contribute to neurodegeneration due to increased neuronal cell death and reduced neurogenesis, reduced remodeling and irreparable damage to the neuronal network, resulting in an enhanced or accelerated brain aging process. In the context of microglia and viral infection, most research has been done in HIV, where the association has been shown for neurocognitive decline [ 127 , 128 , 228 , 246 ]. However, there is little information available about the cellular and molecular mechanisms that contribute to or influence the chronic HIV infection and corresponding involvement of microglia, which requires more future research.…”

Section: Discussionmentioning

confidence: 99%

“…The detailed cellular and molecular mechanisms responsible for HAND have still to be elucidated [ 124 , 125 ]. However, chronic HIV infection results in corresponding neuroinflammation with activation of microglia and astrocytes [ 126 , 127 , 128 ]. There is also increasing evidence that there is production and deposition of beta-amyloid peptide, similar to Alzheimer’s disease [ 129 , 130 ].…”

Section: Virus Infection In the Brainmentioning

confidence: 99%

“…However, microglia may get out of control and out of balance resulting in augmenting brain damage or sustaining chronic pathologies like neuroinflammation and inducing or enhancing neurodegeneration [ 28 , 35 ]. In such case, microglia may enhance brain aging [ 59 , 80 , 128 , 196 , 221 , 222 , 223 , 224 , 225 , 226 ].…”

Section: The Role Of Microglia In Viral Brain Infections Accelerating Brain Agingmentioning

confidence: 99%

See 2 more Smart Citations

The Influence of Virus Infection on Microglia and Accelerated Brain Aging

Filgueira

Larionov

Lannes

2021

Cells

View full text Add to dashboard Cite

Microglia are the resident immune cells of the central nervous system contributing substantially to health and disease. There is increasing evidence that inflammatory microglia may induce or accelerate brain aging, by interfering with physiological repair and remodeling processes. Many viral infections affect the brain and interfere with microglia functions, including human immune deficiency virus, flaviviruses, SARS-CoV-2, influenza, and human herpes viruses. Especially chronic viral infections causing low-grade neuroinflammation may contribute to brain aging. This review elucidates the potential role of various neurotropic viruses in microglia-driven neurocognitive deficiencies and possibly accelerated brain aging.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Virus Infection In the Brainmentioning

confidence: 99%

Section: The Role Of Microglia In Viral Brain Infections Accelerating Brain Agingmentioning

confidence: 99%

See 1 more Smart Citation

The Influence of Virus Infection on Microglia and Accelerated Brain Aging

Filgueira

Larionov

Lannes

2021

Cells

View full text Add to dashboard Cite

show abstract

“…When microglia are activated, the cell body enlarges and the processes contract and thicken [ 22 ]. The activity of microglia was estimated by measuring the rate of stained area of Iba-1 to surface area [ 23 , 24 ]. Photographs of each section were taken and analyzed using an exclusive software (All-in-One Fluorescence Microscope BZ-X710 and BZ-X-Analyzer; KEYENCE Corporation, Osaka, Japan).…”

Section: Methodsmentioning

confidence: 99%

Olanzapine attenuates postoperative cognitive dysfunction in adult rats

Tachi

Fukuda

Tanaka

2021

Heliyon

View full text Add to dashboard Cite

Background: Postoperative cognitive dysfunction (POCD) is associated with poor quality of life and difficulty working. Its impact may be greater in middle-aged patients than in elderly patients. Neuroinflammation is reported to be a main cause of POCD. Olanzapine has been reported to improve learning and memory functions. We therefore investigated olanzapine's effectiveness and mechanisms in an adult rat POCD model. Methods: Six-month-old rats underwent laparotomy and lipopolysaccharide (LPS group) or LPS þ olanzapine (OLA group) intraperitoneal injection or anesthesia alone (CON group) 1 week after a Barnes maze training session. A Barnes maze test trial was then conducted the day after surgery or anesthesia. The microglial activity in the hippocampus and cytokine levels were measured by Iba1 staining and enzyme-linked immunosorbent assay, respectively. Results: The OLA group had significantly higher success rates of Barnes maze trial than the LPS group. The success rate in time of the OLA group was inferior to that of the CON group. On the other hand, the success rate in distance of the OLA group was similar to that of the CON group. Iba1 staining areas in the LPS and OLA groups were larger than that in the CON group; however, the staining area in the OLA group was smaller than that of the LPS group. Plasma interleukin-1β concentration in the LPS and OLA groups was significantly higher than that in the CON group; however, there was no significant difference between the LPS and OLA groups. Conclusion: Olanzapine attenuated both spatial cognitive dysfunction and microglial activity of the hippocampus, which were induced by surgery and LPS injection. These effects were unrelated to inflammatory cytokine concentrations in plasma and hippocampus.

show abstract