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In a demographically diverse sample of healthy people, Cornell researchers found dramatic changes over the human lifespan in the brain’s “blue spot”—a tiny region involved in cognition and believed to be the first affected by neurodegenerative conditions including Alzheimer’s disease.

Using specialized MRI scans to measure the intensity of neuromelanin, a pigment that gives the locus coeruleus (LC) its , the research team observed an inverted U-shaped curve that peaked in later middle age before dropping off sharply, a finding that helps characterize healthy aging patterns.

Maintaining a stronger blue signal after age 60 was associated with better cognitive performance, according to the study involving 134 participants aged 19 to 86. Because of the participants’ diversity, including about 40% who were non-white, the researchers also discovered higher peaks among Black participants and women, groups known to be more susceptible to Alzheimer’s.

As humans age, particularly after middle age, their brain functions, cognitive abilities and memory can deteriorate to varying degrees. Aging-related disorders marked by cognitive decline, particularly dementia, have become increasingly widespread over the past decades.

Estimates suggest that the number of individuals diagnosed with dementia could increase from 55 million in 2019 to around 139 million by 2050. Understanding the factors contributing to and devising methods to detect the first signs of dementia is thus of the utmost importance, as it could help to reliably pick up its emergence and plan therapeutic interventions accordingly.

In recent years, some studies have found a link between people’s ability to perceive and identify odors (i.e., olfactory function) and their cognitive abilities as . While the relationship between and cognitive decline is now well-documented, whether one causes the other or they are the result of similar aging-related or neurodegenerative mechanisms remains unclear.

The magnetization-prepared rapid gradient-echo (MP-RAGE) T1-weighted high resolution structural MRI is a mainstay tool used to identify morphometric biomarkers of disease conditions, progression and treatment effects despite a critical limitation: the relaxation signal on which inferences are based is nearly indistinguishable for gray matter vs. blood flow (Lu et al., 2004; Wright et al., 2008). Thus, apparent reported morphometric findings might be at least partially related to transient changes in blood flow or other physiological signals.

Consistent with this technical limitation, using a standard analysis technique, voxel based morphometry (VBM), we recently reported that a single dose of a medication had “apparent” effects on T1-weighted MRIs (Franklin et al., 2013). Specifically, we observed medication-induced decreases in gray matter volume in the anterior cingulate and other regions that overlapped with changes in brain blood flow (perfusion). Similarly, others have shown effects of medication on T1-weighted scans that are likely transient. For example, acute levodopa administration altered gray matter indices on T1-weighted images in the midbrain (Salgado-Pineda et al., 2006). Further, in a well-controlled longitudinal VBM study of patients with attention deficit hyperactivity disorder (ADHD), Hoekzema et al.

Dismantled’s “Purity” (Vocal Edit) off of their Dystopia CDM (2002)

Feedback surge.
Probe injected.
Data flood overloading neural circuitry.
Trodes on.
Pulse is racing.
Neon grid expanding into binary grey.

We trace our pathways, dissolve in beams.
We breach through cores on static wings.

Pressure starts.
Ice below you.
Shockwaves tumble, pulling.
down the consciousness.
below the circuits.
Noise sets in.
Nervous system failing.
Locked into eternity.
forever looped in frames.

We run through wires, disguise in screens.
We blend in patterns of input streams.

In the previous excerpt from my conversation with Stephen Wolfram, I asked him how I can remain a single, coherent, persistent consciousness in a branching universe.

In this excerpt, we went deeper into this question. As a conscious observer, I have a single thread of experience. So if the universe branches into many timelines, why don’t I branch into many versions of me?

Stephen’s answer touched on many profound aspects of the Wolfram model.

He started with the failure of the Many Worlds interpretation of quantum mechanics to consider the possibility that different branches of history can merge, in other words, come back together again. This failure is rooted in assumption that the universe is continuous; as soon as we start thinking of the universe as discrete, such merging seems not only possible, but inevitable.

He went on to consider the concept of causal invariance, the idea that it doesn’t matter which of countless similar paths you take through the multiway graph, you end up in the same place. In the Ruliad, he said, causal invariance is inevitable.

Then we got to the core of the concept of the observer. According to Stephen Wolfram, an observer equivalences many different states and experiences the aggregate of these states.

In a study published in Science Advances, a research team led by Prof. Liu Chengbo from the Shenzhen Institutes of Advanced Technology (SIAT) of the Chinese Academy of Sciences developed a 1.7-gram head-mounted microscope. This innovative device can simultaneously capture neural activity and cerebral hemodynamics in freely moving mice, providing a novel tool for exploring neurovascular coupling (NVC) in the brain and studying neurological disorders.

NVC represents the close temporal and regional relationship between and and oxygenation. When neural activity is initiated in a specific brain region, the metabolic demand within that region increases, leading to enhanced blood flow to supply greater amounts of oxygen and glucose, thus meeting the elevated metabolic needs of neurons. Conversely, if pathological changes hinder cerebral vessels’ capacity to provide sufficient oxygen and energy, the functional activity of the corresponding brain region will be significantly affected.

Conventional NVC imaging techniques face challenges in achieving simultaneous in vivo high spatiotemporal resolution of neuronal activity and cerebral blood flow. This makes it difficult to accurately capture the dynamic relationship between neural activity and local hemodynamic changes. In addition, most existing studies use head-fixed setups which do not reflect true neurovascular coupling during natural animal behaviors.

Mass General Brigham researchers found that interactions between immune and brain cells drive fear responses, but treatment with psychedelics like MDMA and psilocybin may reverse these effects.

The new study suggests that fear and the immune system are connected in previously unknown ways. The researchers found that the immune system can influence stress and fear behaviors by changing how brain cells communicate.

The investigators further showed that psychedelic treatments could target these neuroimmune interactions and reduce stress-induced fear in preclinical models and found similar results in human . Results are published in Nature.