News
What's happening in Alzheimer's care, research funding, and treatment — summarized simply, each item linked to the original reporting.
Free to read, “May need a subscription” and “Archived copy”: what they mean
Whether an article is free to read is a guess, not a test of your access. Each item is one of three:
- No label: free to read (343 of 400). The publisher’s page marks it free, or the outlet publishes free to read: Medical Xpress, ScienceDaily, NIH (incl. NIA and PMC), Alzheimer's Association, Alzheimer's News Today, NPR, Alzheimer's Disease International, or a .gov site.
- May need a subscription (16 of 400). The publisher’s own page marks the article as not free to read, or — when the page says nothing — the outlet sells subscriptions: The New York Times, STAT, Scientific American, The Washington Post, The Wall Street Journal, Financial Times, The Economist, Bloomberg, The Atlantic, The New Yorker, Wired, Los Angeles Times, The Boston Globe, The Times, The Telegraph, New Scientist, Endpoints News, Science. Each badge says which.
- “Free to read? Not known” (41 of 400). The outlet is on neither list and its page said nothing. We do not call these paywalled.
Archived copy links go to a copy the Internet Archive (web.archive.org) saved, dated the day it was saved. We show one only where the Internet Archive reported a working saved copy when we checked; an archived copy of a subscription article sometimes shows only its opening. 298 of 400 items have one.
Scientists discover a protein that protects the brain from Alzheimer’s damage
A protein called SORLA may act as a powerful defense against the toxic tau tangles involved in Alzheimer’s disease. Mice with extra SORLA had less tau accumulation, less brain atrophy…
Read at ScienceDaily → Archived copy (2 Oct 2026), Internet ArchiveNew Alzheimer's drug repairs DNA damage and reduces brain inflammation
A drug originally developed for spinal cord injury may offer a fresh approach to treating Alzheimer’s disease. In mouse studies, KCL-286 repaired dangerous DNA damage, reduced inflammation…
Read at ScienceDaily → Archived copy (17 Jul 2026), Internet ArchiveThe hidden skeleton “gatekeeper” inside brain cells could help fight Alzheimer's
Researchers have discovered that a microscopic skeleton inside neurons does much more than hold cells together. It acts as a gatekeeper that controls what brain cells absorb and when they absorb it. …
Read at ScienceDaily → Archived copy (15 Jul 2026), Internet ArchiveAlzheimer's tau protein has a surprising secret role in memory
Researchers found that tau is essential for turning new experiences into lasting memories by helping organize the brain's memory-storing cells. …
Read at ScienceDaily →Scientists may have finally found how Alzheimer's kills brain cells
Researchers have identified a previously overlooked mechanism of brain cell death that appears to play a major role in Alzheimer's disease and frontotemporal dementia. …
Read at ScienceDaily → Archived copy (23 Sep 2026), Internet ArchiveScientists may have finally found how Alzheimer's spreads through the brain
A common brain protein may be giving Alzheimer’s disease an unexpected way to spread, carrying toxic Tau proteins from damaged neurons into healthy ones. …
Scientists reprogram brain immune cells to fight Alzheimer’s
A newly identified molecule called OLE helped restore the brain’s immune cells to a more protective state in Alzheimer’s models. The treatment reduced toxic plaque buildup and improved memory, raising hopes for a new therapeutic approach.
Read at ScienceDaily →Scientists May Have Found What Really Triggers Alzheimer’s Disease
Scientists may have uncovered a hidden trigger behind Alzheimer’s disease. Instead of plaques being the root cause, amyloid beta appears to interfere with tau, a protein that helps keep neurons functioning properly. …
Read at ScienceDaily → Archived copy (19 Sep 2026), Internet ArchiveScientists discover a surprising cancer link to Alzheimer’s disease
Researchers discovered that mutations linked to blood cancers may help trigger Alzheimer’s disease by creating overly inflammatory immune cells in the brain. …
Read at ScienceDaily → Archived copy (22 Sep 2026), Internet ArchiveScientists found a new Alzheimer’s trigger and a drug that stops it
Researchers have identified a new Alzheimer’s target and created an experimental compound that blocks a damaging process inside brain cells. In mice, the treatment slowed nerve cell loss, reduced Alzheimer’s-related changes, and even appeared to promote healthier aging.
Read at ScienceDaily → Archived copy (23 Sep 2026), Internet ArchiveScientists found the hidden switch fueling alzheimer’s brain inflammation
Scientists at Scripps Research have uncovered a molecular “switch” that appears to fuel the damaging brain inflammation seen in Alzheimer’s disease. …
Read at ScienceDaily → Archived copy (27 Sep 2026), Internet ArchiveScientists found a hidden Alzheimer’s trigger and shut it down
A newly identified enzyme called IDOL could become a major new target in the fight against Alzheimer’s disease. Researchers found that removing it from neurons sharply reduced amyloid plaques and improved key brain processes linked to resilience and communication between cells. …
Read at ScienceDaily → Archived copy (23 Sep 2026), Internet ArchiveScientists reverse Alzheimer’s in mice with breakthrough nanotechnology
A new nanotechnology treatment reversed Alzheimer’s symptoms in mice by restoring the brain’s natural cleanup system. The specially engineered nanoparticles helped clear toxic amyloid proteins from the brain and repair the blood-brain barrier…
Boosting one protein helps the brain fight Alzheimer’s
Scientists have discovered a way to help the brain clean itself of harmful Alzheimer’s plaques by activating its own support cells. By increasing a protein called Sox9, researchers were able to boost the activity of astrocytes, star shaped cells that help maintain brain health. …
Read at ScienceDaily → Archived copy (2 May 2026), Internet ArchiveScientists restore memory by blocking a single Alzheimer’s protein
Researchers have identified a new potential weapon against Alzheimer’s: blocking a protein called PTP1B. In mice, this approach boosted memory and helped brain immune cells clear harmful plaque buildup. …
Read at ScienceDaily → Archived copy (23 Sep 2026), Internet ArchiveScientists discover Alzheimer’s hidden “death switch” in the brain
Scientists have uncovered a hidden “death switch” in the brain that may be driving Alzheimer’s disease—and even found a way to turn it off in mice. The culprit is a toxic pairing of two proteins that, when combined, triggers the destruction of brain cells and fuels memory loss. …
Read at ScienceDaily → Archived copy (26 Sep 2026), Internet ArchiveScientists turn brain cells into Alzheimer’s plaque cleaners
Scientists have developed a promising new approach to treating Alzheimer’s disease by turning ordinary brain cells into powerful plaque-clearing machines. …
Scientists discover brain switches that clear Alzheimer’s plaques
Researchers have identified two brain receptors that help the brain clear away amyloid beta, a hallmark of Alzheimer’s disease. By stimulating these receptors in mice, scientists increased levels of a natural amyloid-breaking enzyme, reduced buildup in the brain…
Read at ScienceDaily → Archived copy (8 Oct 2026), Internet ArchiveObesity and aging: Study links inflammation to cognitive decline
Obesity and older age are strongly associated with low-grade inflammation in the body, a condition that appears closely linked to cognitive decline and dementia. …
Why it matters: Obesity and older age are linked to low-grade inflammation, which appears closely connected to cognitive decline and dementia.
Read at Medical Xpress → Archived copy (7 Mar 2026), Internet ArchiveBrain 'hazmat' protein cleans up tau: Could it prevent dementia?
Researchers at UC San Francisco have identified a hazardous waste collector in the brain that disposes of the toxic clumps of tau protein that can lead to dementia. Neurons with more of this garbage collector, technically known as CUL5, are less vulnerable to Alzheimer's disease.
Why it matters: UC San Francisco researchers found that neurons with more CUL5, a brain waste collector, are less vulnerable to Alzheimer's disease.
Alzheimer’s may trick the brain into erasing its own memories
Alzheimer’s may destroy memory by flipping a single molecular switch that tells neurons to prune their own connections. Researchers found that both amyloid beta and inflammation converge on the same receptor, triggering synapse loss. …
Read at ScienceDaily → Archived copy (26 Jan 2026), Internet ArchiveScientists find ‘master regulator’ that could reverse brain aging
Researchers have identified OTULIN, an immune-regulating enzyme, as a key trigger of tau buildup in the brain. When OTULIN was disabled, tau vanished from neurons and brain cells remained healthy. …
Read at ScienceDaily →New ALS treatment target identified: STAUFEN-1 protein reduction protects brain cells from death
University of Utah researchers at the Pulst-Scoles Laboratory have discovered that reducing levels of the STAUFEN-1 protein can prevent neuron death caused by DNA damage and p53 activation in neurodegenerative diseases.
Why it matters: Reducing STAUFEN-1 protein levels can prevent neuron death caused by DNA damage and p53 activation in neurodegenerative diseases like ALS.
Read at Medical Xpress →Protective microglia subtype offers potential therapeutic pathway in Alzheimer's disease
In Alzheimer's disease—the leading cause of dementia—microglia, the brain's immune defenders, can act as both protectors and aggressors, shaping how the disease progresses.
Read at Medical Xpress → Archived copy (15 Nov 2025), Internet ArchiveBiological clock based on blood measurements predicts mouse lifespan and frailty
NIA investigators have created a biological clock for mice based on blood measurements. Learn how the clock can help predict differences in aging and how the findings could translate to clinical practice.
Why it matters: NIA investigators created a biological clock for mice based on blood measurements that helps predict differences in aging and could translate to clinical practice.
Read at NIH National Institute on Aging → Archived copy (2 Aug 2026), Internet ArchiveA gene guiding brain cell growth may regulate Alzheimer’s plaque size and toxicity
Plexin-B1 shapes glial networks around beta-amyloid plaques. An NIA-funded study has found that targeting it may improve plaque clearance and reduce brain inflammation.
Why it matters: Targeting Plexin-B1 may improve beta-amyloid plaque clearance and reduce brain inflammation, offering a potential path to regulate Alzheimer's plaque size and toxicity.
Read at NIH National Institute on Aging → Archived copy (2 Oct 2026), Internet ArchiveNew drug candidate targeting synaptic resilience well tolerated in Alzheimer’s patients
A new drug targeting synaptic resilience shows potential in treating Alzheimer’s disease in an NIA-funded study, with early trials indicating safety and possible brain damage reduction. Further research is needed on the drug’s long-term effects.
Why it matters: An NIA-funded study shows a new Alzheimer's drug candidate targeting synaptic resilience is well tolerated in early trials and may reduce brain damage.
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