Significance: It is still unclear why human beings hold higher intelligence than other animals on Earth and which brain properties might explain the differences. The recent studies have demonstrated that biophotons may play a key role in neural information processing and encoding and that biophotons may be involved in quantum brain mechanism; however, the importance of biophotons in relation to animal intelligence, including that of human beings, is not clear. Here, we have provided experimental evidence that glutamate-induced biophotonic activities and transmission in brain slices present a spectral redshift feature from animals (bullfrog, mouse, chicken, pig, and monkey) to humans, which may be a key biophysical basis for explaining why human beings hold higher intelligence than that of other animals.

Alzheimer’s disease (AD), a predominant neurodegenerative disorder, is clinically characterized by progressive cognitive deterioration and behavioral deficits. An in-depth understanding of the pathogenesis and neuropathology of AD is essential for the development of effective treatments and early diagnosis techniques. The neuropathological signature of AD involves two hallmark lesions: intraneuronal neurofibrillary tangles composed of hyperphosphorylated tau aggregates and extracellular senile plaques containing amyloid-β (Aβ) peptide depositions. Although Aβ-centric research has dominated AD investigations over the past three decades, pharmacological interventions targeting Aβ pathology have failed to demonstrate clinical efficacy. Tau, a microtubule-associated protein predominantly localized to neuronal axons, orchestrates microtubule stabilization and axonal transport through dynamic tubulin interactions under physiological conditions. In AD pathogenesis, however, tau undergoes pathogenic post-translational modifications (PTMs), encompassing hyperphosphorylation, lysine acetylation, methylation, ubiquitination, and glycosylation. These PTM-driven alterations induce microtubule network disintegration, mitochondrial dysfunction, synaptic impairment, and neuroinflammatory cascades, ultimately culminating in irreversible neurodegeneration and progressive cognitive decline. This review synthesizes contemporary advances in tau PTM research and delineates their mechanistic contributions to AD pathogenesis, thereby establishing a framework for biomarker discovery, targeted therapeutic development, and precision medicine approaches in tauopathies. This review synthesizes contemporary advances in tau PTM research and delineates their mechanistic contributions to AD pathogenesis, thereby establishing a solid theoretical and experimental basis for the early diagnosis of neurodegenerative diseases, the discovery of therapeutic targets, and the development of novel therapeutic strategies.

Cortex phellodendri is used to reduce fever and remove dampness and toxin. Berberine is an active ingredient of C. phellodendri. Berberine from Argemone ochroleuca can relax airway smooth muscle (ASM); however, whether the nonberberine component of C. phellodendri has similar relaxant action was unclear. An n‐butyl alcohol extract of C. phellodendri (NBAECP, nonberberine component) was prepared, which completely inhibits high K⁺‐ and acetylcholine‐ (ACH‐) induced precontraction of airway smooth muscle in tracheal rings and lung slices from control and asthmatic mice, respectively. The contraction induced by high K⁺ was also blocked by nifedipine, a selective blocker of L‐type Ca²⁺ channels. The ACH‐induced contraction was partially inhibited by nifedipine and pyrazole 3, an inhibitor of TRPC3 and STIM/Orai channels. Taken together, our data demonstrate that NBAECP can relax ASM by inhibiting L‐type Ca²⁺ channels and TRPC3 and/or STIM/Orai channels, suggesting that NBAECP could be developed to a new drug for relieving bronchospasm.

Sphingolipids are essential, complex lipids that are abundant in the cell membranes of eukaryotic cells, particularly concentrated in the myelin and neuronal membranes of the central nervous system (CNS). These lipids are crucial components of the cell membrane, affecting their structure and fluidity, and thus regulating various biological processes, including signal transduction, cell differentiation, apoptosis, and autophagy. The metabolic pathways of sphingolipids are highly complex and conserved, and this metabolic process can produce multiple metabolites. Metabolites such as ceramide (Cer) and sphingosine‐1‐phosphate (S1P) are vital in CNS signaling, affecting neurodevelopment, myelination, and synaptic plasticity. Thus, disruption of sphingolipid metabolism is closely related to neurological disorders. This article provides the latest studies concerning the known features of sphingolipid and sphingolipid metabolism, highlighting its physiological and pathological roles in the CNS.