What makes the human brain distinctive? A new study published in Cell identifies two genes linked to human brain features and provides a road map to discover many more. The research could lead to insights into the functioning and evolution of the human brain, as well as the roots of language disorders and autism.
For decades, one of the most fundamental and vexing questions in neuroscience has been: what is the physical basis of consciousness in the brain? Most researchers favor classical models, based on classical physics, while a minority have argued that consciousness must be quantum in nature, and that its brain basis is a collective quantum vibration of “microtubule” proteins inside neurons.
New research by Wellesley College professor Mike Wiest and a group of Wellesley College undergraduate students has yielded important experimental results relevant to this debate, by examining how anesthesia affects the brain. Wiest and his research team found that when they gave rats a drug that binds to microtubules, it took the rats significantly longer to fall unconscious under an anesthetic gas. The research team’s microtubule-binding drug interfered with the anesthetic action, thus supporting the idea that the anesthetic acts on microtubules to cause unconsciousness.
“Since we don’t know of another (i.e,. classical) way that anesthetic binding to microtubules would generally reduce brain activity and cause unconsciousness,” Wiest says, “this finding supports the quantum model of consciousness.”
Huntington’s disease is an autosomal dominant neurodegenerative disease caused by the repetition of cytosine, adenine, and guanine trinucleotides on the short arm of chromosome 4p16.3 within the Huntingtin gene. In this study, we aim to examine and map the existing evidence on the use of innovations in the rehabilitation of Huntington’s disease. A scoping review was conducted on innovative rehabilitative treatments performed on patients with Huntington’s disease. A search was performed on PubMed, Embase, Web of Science, and Cochrane databases to screen references of included studies and review articles for additional citations. Of an initial 1,117 articles, only 20 met the search criteria. These findings showed that available evidence is still limited and that studies generally had small sample sizes and a high risk of bias.
Habitual coffee consumers justify their life choices by arguing that they become more alert and increase motor and cognitive performance and efficiency; however, these subjective impressions still do not have a neurobiological correlation. Using functional connectivity approaches to study resting-state fMRI data in a group of habitual coffee drinkers, we herein show that coffee consumption decreased connectivity of the posterior default mode network (DMN) and between the somatosensory/motor networks and the prefrontal cortex, while the connectivity in nodes of the higher visual and the right executive control network (RECN) is increased after drinking coffee; data also show that caffeine intake only replicated the impact of coffee on the posterior DMN, thus disentangling the neurochemical effects of caffeine from the experience of having a coffee.
There is a common expectation, namely among habitual coffee drinkers, that coffee increases alertness and psychomotor functioning. For these reasons, many individuals keep drinking coffee to counteract fatigue, stay alert, increase cognitive performance, and increase work efficiency (Smith, 2002). Coffee beverages are constituted of numerous compounds known to affect human behavior, among which are caffeine and chlorogenic acids (Sadiq Butt et al., 2011). From the neurobiological perspective, both caffeine and chlorogenic acids have well-documented psychoactive actions, whereas caffeine is mostly an antagonist of the main adenosine receptors in the brain—A1 and A2A receptors, leading to the disinhibition of excitatory neurotransmitter release and enhancement of dopamine transmission via D2 receptors (Fredholm et al., 2005) to sharpen brain metabolism and bolster memory performance (Paiva et al.
Repetitive reaching tasks in mature female rats triggered persistent pain-like and sickness behaviors linked to a surge in IL-6-driven inflammation throughout muscles, blood, and the brain. These findings reveal how overuse injuries provoke both physical and mood-related symptoms through a neuroimmune cascade.
Brian Kennedy is a renowned biologist, leader in aging research, & director of the Center for Healthy Longevity at the National University of Singapore. In this episode, Brian shares insights from ongoing human aging studies, including clinical trials of rapamycin & how dosing strategies, timing, & exercise may influence outcomes. He presents two key models of aging—one as a linear accumulation of biological decline & the other as an exponential rise in mortality risk—& explains why traditional models of aging fall short. He also explains why most current aging biomarkers lack clinical utility & describes how his team is working to develop a more actionable biological clock. Additional topics include the potential of compounds like alpha-ketoglutarate, urolithin A, & NAD boosters, along with how lifestyle interventions—such as VO2 max training, strength building, & the use of GLP-1 & SGLT2 drugs—may contribute to longer, healthier lives.
View show notes here: https://bit.ly/44ShpRB
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0:00:00-Intro.
0:01:15-Brian’s journey from the Buck Institute to Singapore, & the global evolution of aging research.
0:09:12-Rethinking the biology of aging.
0:14:13-How inflammation & mTOR signaling may play a central, causal role in aging.
0:18:00-Biological role of mTOR in aging, & the potential of rapamycin to slow aging & enhance immune resilience.
0:23:32-Aging as a linear decline in resilience overlaid with non-linear health fluctuations.
0:36:03-Speculating on the future of longevity: slowing biological aging through noise reduction & reprogramming.
0:42:18-The role of the epigenome in aging, & the limits of methylation clocks.
0:47:14-Balancing the quest for immortality with the urgent need to improve late-life healthspan.
0:52:16-Comparing the big 4 chronic diseases: which are the most inevitable & modifiable?
0:57:27-Exploring potential benefits of rapamycin: how Brian is testing this & other interventions in humans.
1:09:14-Testing alpha-ketoglutarate (AKG) for healthspan benefits in aging [1:01:45];
1:13:41-Exploring urolithin A’s potential to enhance mitochondrial health, reduce frailty, & slow aging.
1:17:35-Potential of sublingual NAD for longevity.
1:26:50-Other interventions that may promote longevity: spermidine, 17 HRT, & more.
1:34:33-Biological aging clocks, clinical biomarkers, & a new path to proactive longevity care.
1:45:01-Evaluating rapamycin, metformin, & GLP-1s for longevity in healthy individuals.
1:51:19-Why muscle, strength, & fitness are the strongest predictors of healthspan.
1:53:37-Why combining too many longevity interventions may backfire.
1:56:06-How AI integration could accelerate breakthroughs in aging research.
2:02:07-Need to balance innovation with safety in longevity clinics.
2:10:50-Peter’s reflections on emerging interventions & the promise of combining proven aging compounds.
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About:
The Peter Attia Drive is a deep-dive podcast focusing on maximizing longevity, & all that goes into that from physical to cognitive to emotional health. With over 90 million episodes downloaded, it features topics including exercise, nutritional biochemistry, cardiovascular disease, Alzheimer’s disease, cancer, mental health, & much more.
Peter Attia is the founder of Early Medical, a medical practice that applies the principles of Medicine 3.0 to patients with the goal of lengthening their lifespan & simultaneously improving their healthspan.
A surprising new study has uncovered over 200 misfolded proteins in the brains of aging rats with cognitive decline, beyond the infamous amyloid and tau plaques long blamed for Alzheimer’s. These shape-shifting proteins don’t clump into visible plaques, making them harder to detect but potentially just as harmful. Scientists believe these “stealth” molecules could evade the brain’s cleanup systems and quietly impair memory and brain function. The discovery opens a new frontier in understanding dementia and could lead to entirely new targets for treatment and prevention.