Antibody-mediated enhancement aggravates chikungunya virus infection and disease severity

The arthropod-transmitted chikungunya virus (CHIKV) causes a flu-like disease that is characterized by incapacitating arthralgia. The re-emergence of CHIKV and the continual risk of new epidemics have reignited research in CHIKV pathogenesis. Virus-specific antibodies have been shown to control virus clearance, but antibodies present at sub-neutralizing concentrations can also augment virus infection that exacerbates disease severity. To explore this occurrence, CHIKV infection was investigated in the presence of CHIKV-specific antibodies in both primary human cells and a murine macrophage cell line, RAW264.7. Enhanced attachment of CHIKV to the primary human monocytes and B cells was observed while increased viral replication was detected in RAW264.7 cells. Blocking of specific Fc receptors (FcγRs) led to the abrogation of these observations. Furthermore, experimental infection in adult mice showed that animals had higher viral RNA loads and endured more severe joint inflammation in the presence of sub-neutralizing concentrations of CHIKV-specific antibodies. In addition, CHIKV infection in 11 days old mice under enhancing condition resulted in higher muscles viral RNA load detected and death. These observations provide the first evidence of antibody-mediated enhancement in CHIKV infection and pathogenesis and could also be relevant for other important arboviruses such as Zika virus

Alpha rhythm and Alzheimer\u27s disease: Has Hans Berger\u27s dream come true?

\ua9 2025 The Author(s)In this “centenary” paper, an expert panel revisited Hans Berger\u27s groundbreaking discovery of human restingstate electroencephalographic (rsEEG) alpha rhythms (8–12 Hz) in 1924, his foresight of substantial clinical applications in patients with “senile dementia,” and new developments in the field, focusing on Alzheimer\u27s disease (AD), the most prevalent cause of dementia in pathological aging. Clinical guidelines issued in 2024 by the US National Institute on Aging-Alzheimer\u27s Association (NIA-AA) and the European Neuroscience Societies did not endorse routine use of rsEEG biomarkers in the clinical workup of older adults with cognitive impairment. Nevertheless, the expert panel highlighted decades of research from independent workgroups and different techniques showing consistent evidence that abnormalities in rsEEG delta, theta, and alpha rhythms (< 30 Hz) observed in AD patients correlate with wellestablished AD biomarkers of neuropathology, neurodegeneration, and cognitive decline. We posit that these abnormalities may reflect alterations in oscillatory synchronization within subcortical and cortical circuits, inducing cortical inhibitory-excitatory imbalance (in some cases leading to epileptiform activity) and vigilance dysfunctions (e.g., mental fatigue and drowsiness), which may impact AD patients’ quality of life. Berger\u27s vision of using EEG to understand and manage dementia in pathological aging is still actual

Resting state EEG rhythms as network disease markers for drug discovery in Alzheimer's disease.

Alzheimer's disease (AD) induces a widespread patho-logical extracellular accumulation of beta-amyloid (Ab) peptides that affects cortical networks underpin- ning cognitive functions. This is related to abnormal functional and effective brain connectivity as revealed by graph markers of resting-state eyes-closed electro-encephalographic (EEG) rhythms. Here we revised EEG studies in mild cognitive impairment and AD subjects showing that these markers are promising network disease endpoints for basic research and AD drug discovery