Aberrant ERBB4 in Excitatory Neurons Identified as Key Driver of Alzheimer's Disease Pathology  

A research team led by Associate Director Won-Suk Chung has identified a previously unrecognized driver of Alzheimer's disease (AD): the abnormal expression of the ERBB4 receptor in excitatory neurons, a cell type where this protein is not normally found.

Using single-nucleus RNA sequencing in AD mouse models, the team discovered a distinct population of "early-responsive excitatory neurons" (EREN) marked by ectopic ERBB4 expression—one of the earliest detectable changes during disease progression. Deleting Erbb4 in these neurons reversed hallmark AD features, including abnormal neural activity, synapse loss, glial inflammation, amyloid plaque buildup, and cognitive deficits. Conversely, artificially inducing ERBB4 in healthy neurons was sufficient to trigger these same AD-like changes, even without amyloid plaques.

The team further showed that this effect depends on mTOR signaling downstream of ERBB4, and that the same pathway is active in human AD brain tissue, where it correlates with amyloid burden and cognitive decline.

The findings, published in Nature, point to excitatory neuronal ERBB4 as a promising therapeutic target across Alzheimer's and related neurodegenerative diseases.

Read the full paper: Aberrant excitatory neuronal ERBB4 promotes Alzheimer's disease pathology, Nature (2026)

An article titled “CSF clearance through arachnoid fenestrations to olfactory meningeal lymphatics” has recently been published in Cell

A team led by Dr. Gou Young Koh and Dr. Seon Pyo Hong has found tiny openings in the arachnoid membrane near the olfactory bulbs that let cerebrospinal fluid (CSF) drain directly into lymphatic vessels, which cross the skull's cribriform plate and connect to nasal lymphatics leading to the neck's lymph nodes. Similar structures were confirmed in monkeys.

This drainage route weakens with age, contributing to reduced CSF clearance linked to Alzheimer's and other neurodegenerative diseases. Remarkably, a single intranasal VEGF-C gene therapy fully restored lymphatic function and CSF outflow in aged mice — pointing to a potential treatment strategy.

Nasal ciliated cells are primary targets for SARS-CoV-2 replication in early stage of COVID 19

Lymphatic vessel in lacteal