Exaly – One of my favorite sites, particularly the trends graphs. Makes it easy to see when a particular topic’s research is getting disconnected from citations, an indication that replication/reproduction on the topic is failing. Also super helpful to observe how a topic has grown over time, and current “enthusiasm” for a topic.
Pubpeer – Being a fly on the wall and getting external insight on current research, particularly good for sussing out caveats in research I may not have noticed on my own.
Science hub Mutual Aid community and r/scholar – Useful for getting a sense of what other people are looking at, and often getting exposed to concepts I’d have missed on my own.
Bioarxiv – It’s ugly, it’s clumsy, and it’s messy as hell but it’s still the best way to get a peek 6 months to a year into the future.
PubMed – IMO a much better starting point than Google Scholar, especially with decent search filters set up. It’s the anti-arxiv in that it’s super coherent to use but lacks a lot of the most recent publication.
Libgen – One of the most important sites on the internet. Also.
Research tips: I’m not sure that my research methodologies are unique except for volume, however one of the things I try to do with every article I read is “walk the tree”. Using PubMed, let’s say I just read an article about How the locus coeruleus controls hippocampal “memory” association, and wanted to know if a) there’s other research out there which supports/contradicts it, and b) if there are related functions that can be associated.
In my recommended, I get this article Locus coeruleus activation during environmental novelty gates cocaine-induced long-term hyperactivity of dopamine neurons which I know is going to be partly shit because it’s an “addiction” study, but usually there’s a few pearls available underneath that. Right away reading this, I notice that they immediately start talking about the VTA and provide a few references (VTA and LC are pretty critical nuclei).
One of the first references is to Locus coeruleus and dopaminergic consolidation of everyday memory, which is outside of my recency filter, but provides context and additional information outside of the “addiction” context. And this one also has problems because of it’s obvious small molecule/drug target bias, but taken together we can start to flesh out the boundaries of what this mechanic looks like. Walking through the references in this piece gives us another really interesting piece Pharmacological Dissociation of Novelty Responses in the Human Brain, which is just different enough to expand our information base, but similar enough in context that we gain more boundaries for the circuit mechanic.
Each of these articles has “Similar Articles”, and “Cited By” suggestions. The Cited By articles push us back forward down the tree, and one provides a pretty interesting bit of context In vivo human molecular neuroimaging of dopaminergic vulnerability along the Alzheimer’s disease phases, a current research topic. Now we’ve (very very briefly) walked backwards up the tree amongst the branches and twigs to get a broader sense of the circuit mechanic from different perspectives, now we are going back down the trunk to a more recent article, and get a new sense of how all of this ties together.
From our initial article, we find LC->dCA1 interactions. From our second article, we see that it specifically references consolidation, an extension and confirmation of our initial article. From prior research we understand the “dorsal” stream is external/novelty gated information and this is primarily driven by dopaminergic activity. This indicates that a “ventral” stream must also exist, and the next article which actually experiments with suppressing novelty ties back to our initial article’s findings, showing differential dorsal LC/dope activity from ventral LC/norad activity.
So we understand that the LC has two interdependent streams with differential effects on hippocampal output, how does that tie back to our general dementia/alzheimer’s topic? Well we pop back forward down the tree to find a solid tie to dorsal LC pathology and Alzheimer’s (and outside of this blurb ventral LC and Parkinson’s).
Ultimately the idea isn’t to look for the things we are interested in, it’s to walk back and forth up and down the tree to get an understanding of how the circuits work first, and usually if we have a consistent understanding newer research will ultimately support our research topic (if we are correct). If not, then lack of trunk support means that there was a misunderstanding and we need to refine our circuit understanding.
What this walk did was help us understand that all dementias at least have the same regional origin, and gets us away from being distracted by cerebral etiologies, or hippocampal etiologies or dementia, our understanding of the circuit allows us to know that those are downstream effects of this LC/VTA interaction. We also can infer that the because Alzheimer’s and Parkinson’s (and Huntington’s and ALS) share the same types of insults, they probably aren’t discrete pathologies, but a single class of pathology with differing effect based on insult location.
This becomes really useful because now we understand that every time we read “Alzheimer’s”, the research is probably relevant to all of these other astrocytic metabolic conditions and rescue relevant bits of information together into a more coherent map. Particularly in medical research where every single condition is assumed to be a discrete condition based on some due from 100 years ago who first described it, understanding that all medical conditions derive from similar basis allows much more powerful inferences of function than trying to study every discrete condition by itself.