Happy Valentines Day, from PNAS

[Blog post conceived and written by Kelly Zalocusky, Deisseroth lab] Since the writings of Charles Darwin, female sexual selection has been used to explain flashy-but-costly male traits, from the colorful dances of birds-of-paradise, to the boisterous song of tungara frogs, to the violent posturing of elephant seals. Today in PNAS, researchers from the State University of New York reveal that, at least when it comes to fruit fly pheromones, the effects of this sexual selection are bound by the limits of natural selection. After 7 generations, the prevalence of the gene for high levels of sexy pheromones increased in their mating population from 12% to 35% before hitting a bound and increasing no further. It seems there is a hard limit on the proportion of "sexy" males that can be sustained within a given population.

Sorry ladies.

Happy Valentines Day.

Hine, McGuigan and Blows. Natural selection stops the evolution of male attractiveness. PNAS (2011). DOI: 10.1073/pnas.1011876108

Arsenic Based Life: the story continues

An update to the debate regarding the possibility of bacteria that can incorporate arsenic into DNA and other biomolecules (as described in the recent Science paper by Felicia Wolfe-Simon et al): the first published rebuttal has appeared in the chemical literature (n.b. many thanks to @BoraZ and @bmossop on Twitter for the alert). The rebuttal by Fekry, Tipton and Gates was published in ACS Chemical Biology on January 18th, and examines the potential consequences for DNA's chemical kinetics of a switch from arsenic to phosphate within the backbone structure.  This argument should sound familiar to those who have been following the online debate regarding the Wolfe-Simon's paper, and the article details the problems the GFAJ-1 would need to overcome if it replaced incredibly stable phosphate bonds with inherently unstable arsenate bonds. As quantified by the authors, the half-life of hydrolytic cleavage of the normal phosphate DNA backbone has been estimated as approximately 30 million years. This is in stark comparison with the estimated half-life for hydrolytic cleavage of the proposed arsenate-containing DNA backbone, 0.06 seconds. Such a difference would present a rather extreme challenge for GFAJ-1. As the article notes:

The estimates presented in preceding paragraphs suggest that, if exposed to bulk water, half of the arsenodiester linkages in the genome of Halomonadacea GFAJ-1 would be hydrolytically cleaved in less than 0.1 s. While some bacteria have evolved mechanisms for protecting their DNA under conditions of stress,(36, 37) overcoming such dramatic kinetic instability in its genetic material would be a significant feat for Halomonadacea GFAJ-1. Finally, we note that the use of arsenate esters in cell signaling, enzyme regulation, and cellular respiration would present a similar set of difficulties to the microbe.

This article moves the debate regarding the interpretations of the Wolfe-Simon's paper into arena of the official publication record. It is to be hoped that the original authors will now respond (as they promised to do), thus allowing a somewhat one-sided barrage of criticisms to evolve into a productive scientific discussion.

To celebrate this anticipated shift (and to remind readers of the reported results/interpretations plus major criticisms of the Wolfe-Simon's paper), a video presentation of the article from a recent session of the Stanford Neurosciences Ph.D Program Journal Club.

Unfortunately, the video did not preserve the projected slides as well as expected, so underneath the video readers will find the slides posted (fullscreen view is suggested - an option that can accessed by selecting the Menu button).

Neurosciences Journal Club Presentation Pt 1

Neuroscience Journal Club Presentation Pt 2

Presentation Slides

[slideshare id=6715316&doc=winter2011jc-110126233904-phpapp01]

Predicting Alzheimer's Disease

Welcome to the first Stanford Neuroblog live blogging event of 2011, covering a panel discusion entitled:

Predicting Alzheimer’s Disease: Intersection of Science, Medicine, and Society

From the official description:

We may soon be able, with good accuracy, to tell a healthy 60 year old whether or not he or she will have Alzheimer’s Disease - and, perhaps, how soon the symptoms will appear.  Join our panel of clinicians, lawyers, and health care workers in a discussion about the sciences that may allow us to predict the onset of alzheimer’s disease, and its implications for the health care system, patients, families, and society.

Tonight’s panelists are:

• Hank Greely, J.D. Deane F. and Kate Edelman Johnson Professor of Law; Professor, by courtesy, of Genetics; Director, Center for Law and the Biosciences; Stanford University
• Michael D. Greicius, M.D., M.P.H., Assistant Professor, Department of Neurology and Neurological Diseases, Stanford Medical School; Medical Director, Stanford Memory Clinic
• Michael Gilfix, J.D., expert in Elder Law, Gilfix & La Poll, Palo Alto
• Frank M. Longo, M.D., Ph.D., George E. and Lucy Becker Professor in Medicine; Chair, Department of Neurology and Neurological Diseases; Stanford University

The talk is sponsored by the Stanford Interdisciplinary Group in Neuroscience and Society, the same group that put on the previously blogged panel on Neuroscience in the Courtroom.

The talk begins with Hank Greely opening with a soliloqy regarding the prediction of disease. He notes that disease prediction is nothing new for the human race, and that Alzheimer's Disease (AD) holds a certain resonance, attacking our minds (a scary prospect for most people) as well as being remarkably common. He previews tonights discussion by stating that our ability to predict AD is increasing due to scientific advances. Tonights panel will cover those advances, as well as the effect on patients of this new ability, and both the legal and social implications of an ability to predict AD.

First to speak is:

Dr. Michael Greicius;  Novel Diagnostic and Predictive Tests for Alzheimer's Disease.

Currently, the clinical criteria for probable AD includes: dementia (change in cognition), deficits in two or more cognitive area (visual spatial, memory, etc), progressive decline in memory and other realms (such as executive function), no disturbance of consciousness, onset age 40-90 (mostly 65 and up), and no other explanation. Using these clinical criteria, sensitivity is fairly good , however specificity is rather poor - the distinction being that there are many false positives, but few false negatives. In speciality clinics, diagnosis is accurate 85-90% of the time, which leaves plenty of room for uncertainty. Indeed, the differential diagnosis is rather broad, including mild cognitive impairment, dementia with Lewy bodies, mass lesion, frontotemporal dementia, vascular dementia, depression, and others. Teasing these different possibilites apart can be tricky. For example, take mild cognitive impairment, which can be thought of as a middle ground between normal aging and AD. So a patient with MCI would have memory troubles, but would be able to overcome them. Conversion from MCI to AD is thought to be approximately 12%, and it would be beneficial to have the capability to predict which patients would convert.

Revising AD criteria is ongoing, mostly involving adding biological markers. These markers are preferably diagnostic, predictive, dynamic (tracking the course of the disease, useful as a measure of treatment efficacy), and a gold standard, that it could act as a surrogate for the condition (aka becomes something to treat itself).

Some examples of biological markers:

• Apolipoprotein E (ApoE): polymorphisms, some of which confer risk for AD. It is a susceptibility gene, and is therefore not useful as a general screening tool. However, it may be predictive for how patients will respond to treatment.
• Plaques and Tangles: Beta-Amyloid and Tau. These two proteins are positive markers of AD, that are used in post-mordem confirmation of an AD diagnosis. A group from Pittsburg, Klunk et al, developed a radioactive tracer that can be used to selectively image amyloid plaques in patients. Some limitations are that healthy controls can be positive for the tracer (as high as 51% positivity in health older controls). In addition, amyloid imaging is not dynamic, with signal peaking early in the condition, and not necessarily getting worse during disease progression. In terms of prediction, amyloid imaging is strongly predictive of which MCI patients will convert to AD.
• Spinal fluid markers: Tau is increased and Beta-amyloid is decreased within the spinal fluid of patients - this pattern is predictive in MCI to AD conversion, as well as being sensitive and specific for AD. In addition, a recent study (Fagan et al, Arch Neurol 2007) showed that spinal levels of tau/beta-amyloid can predict the conversion from healthy aging to mild dementia.

Predictive use of biological markers: amyloid imaging is used in selecting people for clinical trials, will soon be used in clinical settings. More ethically dubious is the use of predictive screens for healthy control (this will be covered later in the discussion). Greicius concludes by stating that all the clinical advances are paving the way toward development and early initiation of a definitive AD treatment.

Next to speak is:

Frank Longo, who is discussing the impact of predictive ability on patients.

Longo comments that the ability to predict onset of neurodegenerative diseases is currently available, in the case of Huntington's disease (HD). In the case of HD, genetic testing can confirm with 100% accuracy whether a patient will develop HD during the course of their lifetime. So HD can serve as a model for the ability to apply AD prediction within a clinical setting. Longo describes the protocol for HD genetic testing, saying that it includes genetic counseling, speaking with a trained neurologist, and finally DNA testing, with predetermined follow-up testing. Given a definite protocol, Longo describes his experience with patients, and with the process of giving news. He describes that process that people given a positive prediction for a neurodegenerative disease go through several stages, including resignation, relief because they at least know what the future is bringing, but also highly individualized stress. He describes some of the effects on family and significant others, who are also affected by a positive predictive diagnosis. Longo describes studies on stress in patients given good and bad news regarding their Huntington's diagnosis, saying that generally, data show a general reduction in stress. Longo says that this reduction in stress holds true for positive diagnoses of abnormal BRCA1/2 genes. Longo concludes by stating that the ability to predict AD must be considered in the context of the effect it will have on patients, and patient-family dynamics.

And next is Michael Gilfix.

He will speak as a practicing attorney, who will discuss his experience working with patients and planning of their legal affairs. He notes that the first reaction many patients have is planning for long term medical costs. Proactivity is important, as is applying for government benefits. There appears to be many legal ways to protect personal assets, as well as protocols for transferring legal responsibilities. Gilfix counsels the importance of taking proactive steps while they are still proactive - the sooner a legal plan is in place the better, appears to be his message. He concludes that the advent of predictive testing would allow much more sophisticated planning.

And lastly, Hank Greely takes the podium.

He will discuss the wider societal implications of AD. He starts by noting the differences between HD and AD, primarily the rates of incidence (very low in HD and common in AD) and the distinction between having a risk and knowing for sure (AD or HD, respectively). Now he speaks regarding the topic of regulation of predictive testing. Who will administer the test, who will decide whether any particular test works, who will regulate how the healthcare system will use this predictive information. As he has commented in other discussions, discrimination against those with positive predictive tests will assuredly be an issue. For example, spinal fluid tests are not protected against discriminate as predictive genetic tests are. And even so, employment discrimination against those with positive genetic tests is illegal, which does not mean that it will not happen (see racial and gender discrimination). Furthermore, genetic tests cannot be discriminated against in the realm of health insurance, but not long-term care insurance. In terms of predictive tests that denote "high risk", there are no specific protections against discrimination. He concludes that our society is really unready to handle the consequences of predictive tests for a variety of neurodegenerative conditions.

Question and Answer Session:

Question one, directed to Greicius, regards the cost of the biomarkers for AD, and why he did not recommend more cost-effective tests (such as hippocampal volume)?

Greicius respondes that many of the more cost-effective tests are, in his opinion (and in the opinion of the American Academy of Neurologists), not as accurate as the more expensive diagnostic tests mentioned during his presentation, and cannot be used as a predictive assay for AD.

Question two, mentions the use of calcium channel blockers in an AD mouse model, and asks whether any members of the panel can discuss the study.

Longo responds, saying the calcium channel blockers is just one of many, many drugs that have been shown to be effective in mouse models of AD. Should we use these medications (which are often used in humans to treat other conditions) on the basis of mouse models alone? He notes that no medications identified in mouse models have been shown to be ineffectual in humans, in addition carrying significant side effects.

Question three, what is the youngest age at which tangles/plaques have been identified?

Answer: Perhaps late 40s, early 50s. Patients with Down's Syndrome will have AD by the time they are in their 30's, and will therefore have tangles/plaques at that age. A neuropathologist in the audience points out that although neuropathology is considered the gold standard, there is still a good deal of variation between people in terms of the amount of pathological markers and cognitive deficits. This is probably due to individual differences in susceptibility to the cellular dysfunction and its translation into cognitive phenotype.

Question four: The audience member is concerned about the possibility that not having the test will end up being frowned upon. He asks whether people have thought about mandating privacy regarding results? Greely notes that in terms of genetic testing, employers/insurance companies are not allowed to take into account genetic testing no matter what their status is - and that something similar would probably be required in terms of predictive tests. However he notes that in terms of AD, employers might not care so much, given that people will probably develop AD long after they are no longer working at the company in question.

Question five: How much do these test help us improve accuracy over the current clinical diagnostic tools?

Answer: It ups your likelihood for a correct diagnosis in atypical presentations.

The questions continue as more a discussion, with speakers going too quickly for this typist to capture in any detail. Therefore, I'm ending my coverage, encouraging readers to discuss the panel discussion in the comments.

Linking calcium, oxidative stress, and the role of DJ-1 in Parkinson's disease

PD is a neurodegenerative disease whose defining pathology is the selective degeneration of dopamine producing neurons in an area of the midbrain called the substantia nigra. The biggest mystery in PD research has centered around why these particular neurons degenerate. Research now offers a clue and a tantalizing drug target that may help in treating PD patients. A team led by Dr. James Surmeier, a professor at Northwestern University, has shown that a specific type of calcium channel expressed in substantia nigra dopaminergic neurons may render them more vulnerable to damage by oxidative stress (Guzman et al, 2010). By targeting this channel scientists may be able to develop an entirely new avenue of therapy for PD that would prevent the associated neurodegeneration. The best pharmacological treatment currently prescribed for Parkinson’s disease (PD), the dopamine precursor L-DOPA, was discovered over forty years ago. At best, the administration of L-DOPA can lead to a temporary reprieve from the debilitating motor symptoms associated with PD, but it does not affect disease progression and patients eventually develop a tolerance to it. L-DOPA is still the most widely prescribed medication for PD due to lack of a disease modifying therapy. Dr. Surmeier’s group now offers hope for a new therapy that could block the influx of calcium into dopaminergic (DA) neurons and prevent the progression of PD.

It had been shown previously by the same group that the activity of Cav1.3 (L-type) calcium channels, which allow calcium to enter the cytoplasm of the cell, was not necessary for the functioning of DA neurons, specifically for their pacemaking activity (Guzman et al, 2009). Furthermore, blocking these channels with a chemical called isradipine led to a rescue of DA neuron loss in a neurotoxin mouse model of PD (Chan et al, 2007). So what is it about these channels that is so bad for these highly active DA neurons?

To answer this question, the lead author of the paper, Jamie Guzman, created transgenic mice expressing the redox-sensitive version of GFP (roGFP) under the TH promoter. Upon getting oxidized, roGFP shifts it 490/400 nm excitation spectrum and can be differentiated from non-oxidized roGFP. Furthermore, the construct contained a matrix targeting sequence designed to localize the protein to the mitochondria, which have been centrally implicated in mechanisms of PD pathology. The team then used these mito-roGFP transgenic mice to measure the level of oxidation present in DA neurons from their brains.

Guzman et al found that substantia nigra (SN) DA neurons exhibit a much higher basal level of cellular oxidative stress than DA neurons from the neighboring ventral tegmental area (VTA) which lack these L-type calcium channels. This suggested that Ca2+ influx may somehow be responsible for increased levels of oxidative stress. Indeed when they blocked L-type channels with isradipine, the level of oxidative stress decreased dramatically in SN DA neurons. The research group went on to show that a curious phenomenon, mitochondrial uncoupling, occurs in SN DA neurons as a compensatory mechanism against increased levels of oxidative stress. By uncoupling the mitochondrial electron transport chain from the production of ATP, these neurons are able to reduce the production of toxic reactive oxygen species (ROS) which are a byproduct of the respiratory chain. The authors demonstrated that the uncoupling events, measured by fluctuations in the mitochondrial membrane potential, were dependent on Ca2+ influx and levels of ROS. Again, blocking L-type calcium channels decreased the incidence of these uncoupling events, presumably by reducing oxidative stress levels in the neurons. The data suggests that Ca2+ influx, oxidative stress, and mitochondrial uncoupling are intricately linked together.

The most interesting part of this study was the connection that the authors found between these processes and DJ-1, a protein implicated in Parkinson’s. People with a homozygous loss-of-function DJ-1 mutant genotype develop an early-onset form of PD. To test the role of DJ-1 Guzman et al used a mouse with the DJ-1 gene knocked out. DJ-1 knockout DA neurons exhibited very low levels of mitochondrial uncoupling and correspondingly higher levels of oxidative stress, suggesting DJ-1 might somehow be regulating the mitochondrial response to oxidative stress. Amazingly, blocking the L-type calcium channels completely rescued this oxidative stress effect. Earlier work had implicated DJ-1 in redox signaling pathways and upregulation of antioxidant proteins (Kahle et al, 2009). Thus the authors decided to check whether DJ-1 was exerting it’s effects at the gene expression level. They observed that DJ-1 knockouts had lower transcript levels of some of the key mitochondrial uncoupling proteins, but expression of antioxidant enzymes was unaffected. The authors concluded that a loss of DJ-1 functionality weakened the compensatory mechanisms in mitochondria, making the DA neuron much more vulnerable to oxidative stress in the SN. This may explain why people with homozygous DJ-1 mutations end up suffering from early-onset PD.

The key finding of this study was that the intracellular impairments resulting from a DJ-1 mutation can be reversed by using L-type calcium channel blockers such as isradipine. Isradipine belongs to a class of molecules known as dihydropyridines which are widely prescribed as a treatment for high blood pressure in humans. Perhaps most importantly, these drugs can cross the blood-brain barrier. Recent epidemiological studies support a decreased risk of developing PD in chronic users of dihydropyridines (Becker et al, 2008; Ritz et al, 2010). This offers a ray of hope for PD patients. In fact, clinical trials using isradipine in PD patients have already begun and are in Phase II, with Phase III trials expected to be launched in the next year.

The research by Dr. Surmeier’s group is remarkable in many ways in that it not only elucidated the mechanism underlying the function of a protein implicated in PD, but also identified a drug target and a potential drug candidate that is already in clinical trials. However a lot more needs to be understood about L-type calcium channels and their role in genetic as well as sporadic forms of PD. It may well be that blocking these channels only offers protection in DJ1 knockout and neurotoxin models of PD. Lets keep our fingers crossed that this is not the case.

A link to the Guzman et al study can be found here: http://www.nature.com/nature/journal/v468/n7324/full/nature09536.html

[Mice] Singing in the Lab

Happy New Year everyone! To celebrate the start of 2011, here is a story from the end of last year: "singing" mice.

These mice, generated by a team of Japanese scientists, vocalize in a manner startlingly similar to that of songbirds. These mice are the product of the University of Osaka's Evolved Mouse Project, which screens mice prone to mis-copying DNA for the presence of random mutations. So far, there are no details as to what exact mutation resulted in these mice exhibiting the song-like vocalizations.

For video of the mice, see this Youtube video.

Interestingly, it appears that non-mutant mice do vocalize extensively, just at ultrasonic frequencies (see this video detailing the research of Dr. Christine Portfors). Could the mutation in the Osaka mice be affecting the frequency of mouse vocalizations, reducing them to levels discernible by human ears? Any commentators out there with greater familiarity in songbird and mouse vocalizations, please sing out in the comments.

Stanford Journal Club: Common Ancestry for Mushroom Bodies and the Cortex?

Part of the Stanford Neurosciences curriculum is attendance at a weekly journal club wherein students take turns presenting 30 minute presentations on current or classic papers. Recently, Poh Hui Chia, a 3rd year graduate student in the laboratory of Kang Shen, presented a paper recently published in Cell that used a novel computational technique to examine the possibility that mushroom bodies and vertebrate pallium (aka cortex) could have shared a common ancestor.

The Paper

Profiling by Image Registration Reveals Common Origin of Annelid Mushroom Bodies and Vertebrate Pallium, by Tomer et al, contains a methodologically complex analysis of key cellular and molecular features of both the marine annelid worm, Platynereis' mushroom bodies and the mouse pallium. Those readers with an appreciation for comparative neuroanatomy are sure to enjoy Poh Hui's discussion of the paper's unique computational methods and intriguing results.

In the introduction to their paper, Tomer et al describe the highlights of their paper as follows:

► A new protocol for cellular resolution expression profiling by image registration ► Generation of a multigene map of the developing annelid brain ► The annelid mushroom bodies and the vertebrate pallium share molecular coordinates ► Homology of sensory associative brain centers in Bilateria

JC Presentation Part 1

JC Presentation Part 2

Abstract

From Tomer et al, 2010:

The evolution of the highest-order human brain center, the “pallium” or “cortex,” remains enigmatic. To elucidate its origins, we set out to identify related brain parts in phylogenetically distant animals, to then unravel common aspects in cellular composition and molecular architecture. Here, we compare vertebrate pallium development to that of the mushroom bodies, sensory-associative brain centers, in an annelid. Using a newly developed protocol for cellular profiling by image registration (PrImR), we obtain a high-resolution gene expression map for the developing annelid brain. Comparison to the vertebrate pallium reveals that the annelid mushroom bodies develop from similar molecular coordinates within a conserved overall molecular brain topology and that their development involves conserved patterning mechanisms and produces conserved neuron types that existed already in the protostome-deuterostome ancestors. These data indicate deep homology of pallium and mushroom bodies and date back the origin of higher brain centers to prebilaterian times.

Profiling by Image Registration Reveals Common Origin of Annelid Mushroom Bodies and Vertebrate Pallium. Tomer et al (2010). Cell 142(5): 800-809.

U Can't Touch This

Another epic moment in PubMed searches, presented without comment. [Courtesy of Stanford graduate student Geeorge Sebastià Vidal Pérez-Treviño.]

SFN: Robert Wurtz's Lecture - A perspective

The neural basis of cognitive phenomena: are monkeys the ideal model?Sridhar Devarajan

In his presidential special lecture delivered to the Society for Neuroscience (Nov.15, 2010), Prof. Robert Wurtz highlighted the importance of non-human primates (monkeys) in cognitive neuroscience research. Monkeys can be trained on a variety of complex behaviors, and exhibit brain structures that are remarkably homologous to the human brain. While acknowledging that the choice of model organism should be driven by the research question, Prof. Wurtz underscored the special status of monkeys as the model of choice for understanding the neural basis of cognitive phenomena, such as attention.

While appealing, this argument begs the question: are such cognitive phenomena unique to primates? Take attention, for instance. Attention control in primates is known to be of two kinds: “goal-directed” and “stimulus-driven”. During the performance of a demanding task, we engage our attention on task-relevant stimuli in a “goal-directed” fashion. For instance, when driving to a friend’s place in an unfamiliar neighborhood, our attention is closely engaged in tracking street signs and other relevant landmarks, while ignoring irrelevant details of the landscape. On the other hand, unexpected and highly salient stimuli automatically draw (capture) our attention (“stimulus-driven”). For instance, a sudden, loud siren immediately draws our attention to the approaching fire truck, so we can get out of its way quickly, if need be.

How certain are we that similar kinds of attention control do not operate in the brains of other classes of (non-primate) animals? How about insects? Bees, for example, forage for nectar-bearing flowers matching a specific sensory template while carefully avoiding physically similar, but irrelevant objects. On the other hand, a sudden bright light, or a loud noise startles bees and quickly draws their (collective) attention to the source of the disturbance, as many a gardener who has accidentally disturbed a beehive could painfully attest. Hence, it is difficult to assert that similar forms of “goal-directed” and “stimulus-driven” attention control do not operate in the primitive insect brain.

Do insects share other “cognitive” phenomena besides "attention"? How about "motivation"? Symbolic communication? Learning? Memory? Perception? Where can we draw the line in the animal kingdom in terms of these phenomena? And where does this leave us with regard to the original question: Are monkeys indeed the ideal model for understanding the neural bases of cognitive phenomena?

Prof. Bob Wurtz’s assertion is relevant for cognitive neuroscientists who wish to understand the mechanistic basis of cognitive phenomena in the human brain. Indeed, such knowledge is fundamental to diagnose and treat cognitive disorders (such as schizophrenia, and autism) that afflict the human brain, and for which no cures are currently available. However, from a basic science perspective, Prof. Wurtz’s proposal leaves little room for understanding the emergent principles of brain circuits and their computations that give rise to cognitive phenomena, such as attention.

An analogy, might help illustrate this distinction. I have had the unique experience of trying to figure out the rules of American football by watching two professional teams compete. While I broadly understood that each team’s objective was to get the ball across the opponents' line at the other end of the field, the gameplay proceeded so quickly, and with such intricately complex maneuvers, that I completely failed to decipher the essential rules: the rules of passing, the concept of a “first-down” and the like. The fact that the players on the field appeared to  transform, without warning, into a completely different set of individuals did not help either. Perhaps, it would have been easier for me to figure out these essential rules, had I observed the simpler gameplay of middle schoolers less encumbered by advanced, and complex strategies.

A basic goal of cognitive neuroscience is to understand core principles by which cognitive phenomena arise in the intricate wetware of the brain. Prematurely restricting study of the neural basis of cognition to specific animal models raises the potential risk of "overfitting", of failing to unravel fundamental principles of neural circuit operation that give rise to such phenomena.

Molecular Animation: Cinematic Science

From the animators that brought us the glorious video, The Inner Life of the Cell in 2006, comes another tour de force in molecular animation. This time, the collaborative team of BioVisions, a scientific visualization program at Harvard’s Department of Molecular and Cellular Biology, and the Connecticut-based scientific animation company Xvivo have created a video entitled Powering the Cell: Mitochondria.

As with their previous video, Powering the Cell: Mitochondria is a glorious depiction of intricate cellular processes that combines detailed science with beautiful animation. Both videos can be seen below (Inner Life after the break), and the field of scientific animation can be learned about by reading the recent NYTimes article of molecular animation.

Powering the Cell: Mitochondria

The Inner Life of the Cell