A groundbreaking study reveals the crucial role of the protein p62 in reducing neurodegenerative disorders through selective autophagy. Cells use selective autophagy or self-degradation of undesired proteins to maintain cellular homeostasis (i.e., a state of balance). This process is controlled by
Dementia models revealed that the p62 receptor protein can help protect the brain against dementia.
Tau proteins, which play a crucial role in the internal architecture of neurons in the brain, abnormally accumulate within neurons in disorders such as dementia anddisease. This accumulation of hyperphosphorylated tau proteins in the brains of dementia patients leads to the creation of neurofibrillary tangles and eventually cell death of neurons, leading to the disease’s progressive neurodegenerative symptoms.
Maiko Ono states, “This protein’s ubiquitin-binding ability helps in the identification of toxic protein aggregates , which can then be degraded by cellular processes and organelles.” MRI scans revealed that the hippocampus of p62 KO mice was degenerated and inflamed. A postmortem assessment of their brains revealed a greater loss of neurons in their hippocampus. Further immunofluorescent studies showed that the abnormal tau species aggregates can cause cytotoxicity leading to inflammation and cell death of neurons in p62 KO mice. Oligomeric tau, specifically, accumulated more in the brains of p62 KO mice.
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