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 (335 of 388). 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 (15 of 388). 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” (38 of 388). 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. 278 of 388 items have one.
First atlas tracks proteins that cross the blood-brain barrier
Your brain is protected by the blood-brain barrier—a network of cells in the brain's blood vessels that serves as a border between the brain and the rest of your bloodstream. …
Read at Medical Xpress →Brain activity patterns may predict Alzheimer's years before memory slips
Inside the brains of some cognitively normal adults, firing patterns were able to foretell Alzheimer's disease years before the onset of memory loss or the accumulation of plaques and tangles, according to new Stanford Medicine–led research. …
Read at Medical Xpress →Rapid tau spread may explain why midlife Alzheimer's progresses more rapidly
Patients with early-onset Alzheimer's disease, whose symptoms start before age 65, have more extensive deposits of tau, a hallmark protein of the condition, compared with patients whose symptoms start at 65-plus, a new study found. …
Read at Medical Xpress →Hidden ancestral links found in motor neuron disease and dementia could speed up gene discovery
Researchers at the Macquarie University Brain Institute and Clinic have helped accelerate the search for disease-causing genes by building new genetic 'families.' …
Read at Medical Xpress →Mouse study reveals molecular link between high-fat diets and impaired brain function
The molecular mechanisms linking a high-calorie diet to cognitive impairment remain unclear. Researchers at the Institute of Science Tokyo, Japan, investigated this association in mice…
Read at Medical Xpress →New microscopy technology may help detect neurological diseases before neurons die
Scientists studying amyotrophic lateral sclerosis (ALS), Parkinson's, Alzheimer's and other neurological diseases are getting unprecedented views inside brain cells, using powerful new microscopes to uncover changes that may begin long before neurons die. …
Read at Medical Xpress →Lab-designed molecule reduces amyloid beta, the protein linked to Alzheimer's disease, in mice
A research team led by the Molecular and Cellular Neurobiotechnology group at the Institute for Bioengineering of Catalonia (IBEC), in collaboration with Míriam Royo's laboratory at the Institute for Advanced Chemistry of Catalonia (IQAC-CSIC)…
Read at Medical Xpress → Archived copy (29 Oct 2026), Internet ArchiveResearchers restore neuron function in mice with Alzheimer's disease
Researchers were able to restore the function of neurons linked to cognitive function and information processing in mice that mimic key features of Alzheimer's disease, showing early promise for the development of a similar targeted therapy in humans. …
Read at Medical Xpress →Who gets Alzheimer's drugs? Race, vulnerability and health status shape access
The first disease-modifying drugs for Alzheimer's disease offer patients the ability to slow cognitive decline by targeting amyloid plaques in the brain. But a new study suggests that not all patients have the same opportunity to receive these treatments.
How the biggest Alzheimer's risk gene disrupts the process of insulating neurons
One of the main ways that the APOE4 gene variant, the biggest genetic risk factor for late-onset Alzheimer's disease, undermines brain circuit function is by disrupting the process of insulating neurons with a fatty sheath that optimizes their electrical transmission.
Read at Medical Xpress → Archived copy (16 Oct 2026), Internet ArchiveBrain-protective molecule may help preserve memory during aging
As humans age, both protective and harmful biological processes shape brain health. When the balance shifts in favor of harmful processes, age-related changes in the brain can accelerate, including synapse loss, disruptions in lipid metabolism and chronic inflammation.
Read at Medical Xpress → Archived copy (18 Oct 2026), Internet ArchiveMolecular glue degraders show early promise in reducing Alzheimer's-linked brain plaques
A research team led by Indiana University School of Medicine scientists has discovered a new method for reducing the formation of amyloid plaques…
Read at Medical Xpress → Archived copy (15 Oct 2026), Internet ArchiveThe shape of water at a key tau hotspot helps drive dementia-linked clumping
Diseases such as Alzheimer's and frontotemporal dementia are considered neurodegenerative tauopathies, in which tau proteins in the brain misfold and lead to cognitive decline. …
Read at Medical Xpress → Archived copy (13 Oct 2026), Internet ArchiveStudy offers new clues about how genetic risk for Alzheimer's affects brain immune cells
Researchers at the University of Colorado Anschutz and Pacific Northwest National Laboratory have found a new clue that may help explain why some people are more likely to develop Alzheimer's disease. …
Read at Medical Xpress → Archived copy (13 Oct 2026), Internet ArchiveDrug combination that reduces oxygen levels in tissues improves Parkinson's symptoms in mice
In a new study, Broad Institute researchers report that two small-molecule chemicals that reduce oxygen delivery to cells improved symptoms of neurodegeneration in a mouse model of Parkinson's disease. …
Read at Medical Xpress →Increasing protective protein suppresses Parkinson's-linked buildup, more than doubling lifespan in mouse model
Parkinson's disease is the second most common neurodegenerative disease. Over the last 30 years, studies have shown that a protein called alpha-synuclein abnormally aggregates in people with Parkinson's disease…
Read at Medical Xpress → Archived copy (13 Oct 2026), Internet ArchiveManaging misfolded proteins to prevent Parkinson's disease
The protein alpha-synuclein is abundant in healthy brains and plays an important role in enabling communication between nerve cells. However, under certain conditions, misfolded alpha-synuclein proteins can accumulate into toxic clumps inside neurons. …
Read at Medical Xpress →Brain tissue removed during surgery reveals potential way to curb inflammation linked to Alzheimer's
Inflammatory conditions in the brain, including traumatic brain injury and degenerative diseases like Alzheimer's, could be targeted with an existing drug thanks to new research that shows it can work in brain cells.
Why it matters: New research in brain cells reveals an existing drug could potentially curb inflammatory conditions linked to Alzheimer's and traumatic brain injury.
Read at Medical Xpress → Archived copy (8 Oct 2026), Internet ArchiveHuman tau seeds trigger disease-specific shapes in mouse brains, new study finds
Tau is a protein that occurs naturally in the brain. It is essential for proper neuron development and for how neurons communicate with each other. The same protein, however, when misshapen or misfolded, can act as a driver of neurodegenerative diseases. …
Why it matters: Misshapen tau protein can act as a driver of neurodegenerative diseases despite its natural role in neuron development and communication.
Read at Medical Xpress → Archived copy (5 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.
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 ArchiveFollow new items in a feed reader: Atom feed.