For individuals with Alzheimer disease (AD), the emergence of psychosis is associated with elevations in levels of plasma tau phosphorylated at threonine 181 (p-tau181), according to a study published online June 26 in JAMA Psychiatry.

Jesus J. Gomar, Ph.D., and Jeremy Koppel, M.D., from the Feinstein Institutes for Medical Research in Manhasset, New York, examined the longitudinal dynamics of p-tau181 and neurofilament light chain protein (NfL) levels in association with the emergence of psychotic symptoms. Patients with mild cognitive impairment (MCI) and AD (with psychosis [AD+P] and without psychosis [AD−P]) and participants who were cognitively unimpaired (CU) were compared at baseline.

For the longitudinal analysis, participants with MCI and AD were categorized into those with evidence of psychosis at baseline and those who showed incidence of psychosis over the course of the study. The cohort included 752 participants with AD and 424 CU participants.

Learning and memory impairments in a Down syndrome mouse model were reversed by correcting expression of a gene that influences the generation of new neurons in the brain. The finding could pave the way to treat the cognitive impairment associated with the syndrome in humans.

Adult neurogenesis is the process of generating new neurons in the adult brain. Defects in this process have been observed in various animal models of neurological disorders including schizophrenia, depression, Parkinson’s disease, Alzheimer’s disease, and neurodevelopmental disorders such as Down syndrome. But the precise cellular and molecular mechanisms underlying adult neurogenesis and their links to neurological disorders are not well understood.

Molecular neurobiologist Kyung-Tai Min at Korea’s Ulsan National Institute of Science and Technology and his colleagues found that interactions between a gene called the Down syndrome critical region 1 (DSCR1) and two other molecules, TET1 and miRNA-124, were necessary for adult neurogenesis and were important in learning and memory.

Sam Parnia, associate professor at New York University, suggests that death can be reversed and our brains may remain salvageable for hours or days after death. He emphasizes that death can be viewed as an injury process, with the potential for revival through ECMO machines and specific drugs used in CPR cocktails to aid recovery.

In a world-first, scientists have figured out how to reprogram cells to fight — and potentially reverse — brain diseases like Alzheimer’s.

Researchers at the University of California, Irvine created lab-grown immune cells that can track down toxic brain buildup and clear it away, restoring memory and brain function in mice.

They did this by turning stem cells — which can become any cell in the body — into brain immune cells called microglia.

Patients with spastic paraplegia type 15 develop movement disorders during adolescence that may ultimately require the use of a wheelchair. In the early stages of this rare hereditary disease, the brain appears to play a major role by over-activating the immune system, as shown by a recent study published in the Journal of Experimental Medicine.

The study was led by researchers at the University of Bonn and the German Center for Neurodegenerative Diseases (DZNE). These findings could also be relevant for Alzheimer’s disease and other neurodegenerative conditions.

Spastic paraplegia type 15 is characterized by the progressive loss of neurons in the central nervous system that are responsible for controlling movement. Initial symptoms typically appear in late childhood, manifesting first in the legs in the form of uncontrollable twitching and paralysis.

Although the brain is our most complex organ, the ways to treat it have historically been rather simple.

Typically, surgeons lesioned (damaged) a structure or a pathway in the hope that this would “correct the imbalance” that led to the disease. Candidate structures for lesioning were usually found by trial and error, serendipity or experiments in animals.

While performing one such surgery in 1987, French neurosurgeon Alim-Louis Benabid noticed that the electrical stimulation he performed to locate the right spot to lesion had effects similar to the lesion itself.

Parkinson’s disease is a neurodegenerative disorder that is usually diagnosed in its late stage on the basis of clinical symptoms, mainly motor disorders. By this point, however, the brain is already severely and irreparably damaged. Moreover, diagnosis is difficult and often incorrect because the disease takes many forms, and symptoms overlap with other disorders.

Researchers from the PRODI Center for Protein Diagnostics at Ruhr University Bochum, Germany, and the biotech company betaSENSE have now discovered a biomarker in the spinal fluid that facilitates a reliable diagnosis at an early stage and can shed light on the progression of the disease and the effect of a therapy. They report their findings in the journal EMBO Molecular Medicine from April 25, 2025.