The important immune cells in the brain are called microglia acting as the central junction between neuroinflammation and neurodegenerative diseases. In patients of cognitive disorders and Alzheimer’s disease (AD) animal models, amoebic morphology and inflammatory pathways are activated to release numerous cells in the inflammatory factors by active microglia.

Current research investigating the pathomechanisms of neurodegenerative disorders of the central nervous system (CNS), such as Alzheimer’s disease (AD), amyotrophic lateral sclerosis (ALS), or Parkinson’s disease (PD), led to the understanding that these diseases have to be seen in the context of immune responses. In other words, inflammation plays a central role in neurodegenerative disorders of the CNS. 

Conformational changes of Tau have been described to occur during its fibrillary and non-fibrillary aggregation inside neurons affected in the brain of Alzheimer’s disease (AD) patients. Two consecutive conformations have been described during the progression of the disease: an early conformation detected with the Alz-50 antibody, recognizing Tau molecules folding its amino terminus over its third repeated domain, and a later conformation involving the bending of the proline-rich region over the third repeated domain.

Alzheimer’s disease (AD) remains a formidable challenge in neuroscience, with its complex pathology still lacking an effective cure. Recent research has highlighted the critical role of epigenetic regulation in AD, demonstrating how environmental factors and genetic predispositions influence disease progression at a molecular level. This commentary examines key advancements in AD-related epigenetic research, with a particular focus on histone deacetylases (HDACs) and adrenergic signaling-two mechanisms that have emerged as promising therapeutic targets for mitigating AD symptoms and slowing neurodegeneration.

Monoamine oxidase B (MAO-B) is a mitochondrial enzyme predominantly expressed in astrocytes, where it plays a crucial role in neurotransmitter metabolism, oxidative stress regulation, and neuroinflammation. In addition to its well-characterized function in the oxidative deamination of monoamines such as dopamine, noradrenaline, and serotonin, MAO-B is increasingly recognized for its involvement in astrocytic GABA synthesis.