Although the fact is often forgotten, the American colonists were not the only people who faced a political crisis in the late 18th century. The British people did too. And, ironically, the United States finds itself in a situation today very similar to the one Britain faced back then.
The diagnostic checklist that an attentive observer might have drawn up in Britain in the 1770s seems very familiar. The constitution was out of balance, and the executive—at this time still the King—was accumulating powers and patronage at the expense of Parliament.
…The radicals in Britain pursued two chief goals: reform to the Civil List, and the establishment of universal male suffrage. Both had the purpose of reining in corruption…. Richmond introduced a suffrage bill in 1780. Although it failed, it became the basis for political efforts that built consistently over the next 50 years…. In the end, over the course of nearly a century, there would be four Reform Acts. The last, in 1918, finally delivered universal male suffrage, as well as suffrage for many women. A decade later, the vote was extended to all women.
Of course, this is not exactly the situation we find ourselves in today. But the struggle for government of, by, and for the people was followed for decades, and ultimately was pretty successful. Interesting reading!
2,500 words: https://www.theatlantic.com/ideas/2026/05/18th-century-britain-reform/687221/. If this is paywalled for you, contact me.
Good news from Fix the News (long one, this could have been a post all by itself):
The past year has brought us three Alzheimer’s breakthroughs. For 30 years, Alzheimer’s research has had one song, “Amyloid plaques are bad.” Billions of dollars, two FDA-approved drugs (lecanemab and donanemab), and yet Alzheimer’s patients have only gotten slightly less worse, a little bit slower. But within the last 12 months, three separate teams have said: what if we tried literally anything else.
Indiana University went for an enzyme called IDOL. Everyone assumed it mattered in the brain’s immune cells because that’s where most of it gets made. Wrong floor. Knock out IDOL in neurons and plaques drop, APOE (the gene variant that’s basically a lit fuse for late-onset Alzheimer’s) drops, and the receptors that keep neurons talking to each other go up.
Barcelona, Sichuan and London ignored the neuron, and went for the plumbing instead. The blood-brain barrier has a protein called LRP1 whose job is grabbing amyloid and shoving it into the bloodstream — except in Alzheimer’s, LRP1 jams. They built nanoparticles that act like a reset button. Three injections, and an elderly mouse came out behaviourally indistinguishable from a healthy one.
Bordeaux, Moncton and Inserm went one floor deeper. Forget the neurons, forget the plumbing, look at the power supply. Mitochondria — the engines inside every neuron — start failing before cells die. So the team built an artificial receptor that revs them back up, and memory came back.
Caveat: Mice. It’s always mice. But it looks like the amyloid plaque monopoly might finally be over.
And an image from my collection:




