Brain preservation is an effort to preserve memories with the intent to revive the person in the distant future.
Enzymes are the molecular machines that power life; they build and break down molecules, copy DNA, digest food, and drive virtually every chemical reaction in our cells. For decades, scientists have designed drugs to slow down or block enzymes, stopping infections or the growth of cancer by jamming these tiny machines. But what if tackling some diseases requires the opposite approach?
Speeding enzymes up, it turns out, is much harder than stopping them. Tarun Kapoor is the Pels Family Professor in Rockefeller’s Selma and Lawrence Ruben Laboratory of Chemistry and Cell Biology. Recently, he has shifted the focus of this lab to tackle the tricky question of how to make enzymes work faster.
Already, his lab has developed a chemical compound to speed up an enzyme that works too slowly in people with a rare form of neurodegeneration. The same approach could open new treatment possibilities for many other diseases where other enzymes have lost function, including some cancers and neurodegenerative disorders such as Alzheimer’s.
The devastating illness deteriorates your brain’s ability to think, remember things and can even alter your behaviour.
While some studies have discovered that engaging in a pretty gross habit or reaching a daily step count can reduce the risk of developing Alzheimer’s disease (AD), for over a century, scientists have considered it an irreversible illness. This is why research has focused on preventing or slowing its progression, rather than recovery.
However, a new study challenges this long-held belief by testing whether brains already severely afflicted with advanced AD could recover.
Inside the body, a 24-hour rhythm, known as the circadian rhythm, quietly coordinates when we sleep, wake, eat, and recover. This internal timing system helps keep organs and hormones working in sync.
When it becomes disrupted, the effects may extend well beyond poor sleep, with growing evidence suggesting consequences for long-term brain health.
A large 2025 study of more than 2,000 people with an average age of 79 found that those with a strong circadian rhythm had an almost halved risk of developing dementia. Circadian rhythms regulate daily processes, including sleep timing, hormone release, heart rate, and body temperature.
To assess how this interaction affected development, the team compared gene expression in the cortical region of the assembloid with that of a standalone cortical organoid. The cortical tissue connected to the thalamus showed signs of greater maturity, indicating that thalamus cortex communication promotes cortical growth and development.
Thalamic Signals Drive Neural Synchrony
The scientists also examined how signals traveled through the assembloid. They found that neural activity spread from the thalamus into the cortex in wave like patterns, creating synchronized activity across cortical networks.
University of Florida neuroscientists have made a mechanistic discovery that paves the way to test immune-modulating medicines as a potential tool to break the cycle of methamphetamine addiction.
In a new preclinical study, a McKnight Brain Institute team led by Habibeh Khoshbouei, Ph.D., Pharm. D., examined the role of neuroinflammation in meth addiction to provide a deeper understanding of the mechanisms at work.
“Unlike alcohol or opioids, there currently is no medicinal therapeutic approach for methamphetamine addiction,” said Khoshbouei, a professor of neuroscience and psychiatry. “So this is an important societal issue.”
Parkinson’s disease (PD) is a debilitating and progressive neurodegenerative disorder caused by the loss of dopamine-producing neurons in the substantia nigra, a brain region essential for motor control. Clinically, it is marked by tremor, rigidity, bradykinesia and postural instability, symptoms that progressively erode independence and quality of life.
PD affects millions of people worldwide, including nearly one million individuals in the United States, making it one of the fastest-growing neurological disorders. In the U.S. alone, the disease imposes a profound health care and socioeconomic burden, with annual costs reaching tens of billions of dollars due to medical care, lost productivity and long-term disability.
While environmental factors contribute to disease risk, genetic drivers are increasingly recognized, with mutations in the leucine-rich repeat kinase 2 (LRRK2) gene representing one of the most common causes of both familial and sporadic PD. Understanding how LRRK2 mutations drive disease is therefore central to developing therapies that go beyond symptoms control.
A new study from Karolinska Institutet, published in Nature Communications, reveals how rhythmic brain waves known as alpha oscillations help us distinguish between our own body and the external world. The findings offer new insights into how the brain integrates sensory signals to create a coherent sense of bodily self.
What makes you feel that your hand is yours? It might seem obvious, but the brain’s ability to tell self from non-self is a complex process.
Using a combination of behavioral experiments, brain recordings (EEG), brain stimulation, and computational modeling with a total of 106 participants, researchers from Karolinska Institutet investigated how the brain combines visual and tactile signals to create the feeling that a body part belongs to oneself—a phenomenon known as the sense of body ownership.