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GLP-1 drugs like semaglutide (Ozempic, Wegovy) showed promise in preclinical studies for Alzheimer’s disease (AD) due to neuroprotective effects. Recent large-scale clinical trials have found they do not slow disease progression or improve cognition in early AD, disappointing initial hopes. Researchers remain cautiously optimistic about potential future uses, possibly in combination treatments or different formulations, but current data suggest metabolic improvements alone aren’t enough to stop cognitive decline.

Addressing the dysfunctions of all brain cell types in Alzheimer’s disease (AD) should cure the dementia, an objective that might be achieved by GLP-1 agonist drugs, because receptors for GLP-1 are present in all of the main brain cell types, i.e., neurons, oligodendroglia, astroglia, microglia, endothelial cells, and pericytes. This article describes the benefits provided to all of those brain cell types by GLP-1 agonist drugs. The article uses studies in humans, not rodents, to describe the effect of GLP-1 agonists upon cognition, because rodents’ brains differ from those of humans in so many ways that results from rodent studies may not be totally transferable to humans.

Commercially available GLP-1 agonists have mostly shown either positive effects on cognition or no effects. One important reason for no effects is a reduced rate of entering the brain parenchyma. Dulaglutide has the greatest entry to the brain, at 61.8%, among the available GLP-1 agonists, and seems to offer the best likelihood for the cure of AD. Although there is only one study of cognition that used dulaglutide, it was randomized, placebo-controlled, and very large; it involved 8828 participants and showed a significant benefit to cognition. A clinical trial to test the hypothesis that dulaglutide may cure AD should have, as its primary outcome, a 30% greater cure rate of AD by dulaglutide than that achieved by an equipoise arm of, e.g., lithium plus memantine.

GLP-1 agonists, Alzheimer’s dementia, cure, brain cells
Cure should be the goal of therapy for Alzheimer’s dementia (AD). One approach is to address all of its major causal factors, but that requires the administration of an unfeasible number of drugs. Since the ultimate, underlying cause of the dementia is dysfunction of brain cells, addressing all of those dysfunctions is another approach to curing it; using that approach, GLP-1 agonists may cure the dementia because, as shown below, all of the major, dysfunctional brain cell types in AD, including neurons, oligodendroglia, astrocytes, microglia, endothelial cells, and pericytes, express receptors for the glucagon-like peptide 1.

The account by Holst provides a brief introduction to the 30-amino acid peptide hormone, glucagon-like peptide 1 . GLP-1 is a product of the glucagon gene. The primary translation product, proglucagon, a peptide of 160 amino acids, contains, apart from the glucagon sequence, two glucagon-like sequences designated GLP-1 and GLP-2. They are glucagon-like because, with respect to amino acid sequence, they are about 50% homologous to glucagon. When the prohormone is processed, the glucagon sequence is cleaved out, whereas the part containing the GLPs is secreted as a single, large peptide”.

GLP-1 and Brain Cells
GLP-1 agonists have been extensively studied in relation to their effect on energy metabolism and nutrition. In that respect, and a link with GLP-1, a risk factor for developing AD is being underweight, a condition that is countered by GLP-1 agonists. In fact, the nutritional status of AD patients is significantly compromised and tends to worsen with the progression of AD. Further links between a GLP-1 agonist and AD are the facts that a disturbed circadian rhythm occurs in AD, that blood levels of circadian clock proteins are increased in sleep apnea [6], and that the GLP-1 agonist, tirzepatide, benefits sleep apnea. GLP-1 receptors exist in various brain regions, including the nucleus accumbens and the brainstem. GLP-1-activated paraventricular signaling mounts a whole-organism response to stress. Data in the following sections show GLP-1 receptors in all brain cell types.

GLP-1 and Neurons
GLP-1 is widely present in the brain, where it is neuroprotective by reducing neuronal apoptosis and by promoting both neurite outgrowth and synaptic plasticity. The neuronal marker c-fos shows neuroanatomical connections, and enabled the demonstration that peripherally administered GLP-1 increased neuronal expression in the brainstem and amygdala. GLP-1 receptors are abundant in the c-brain stem, where preproglucagon neurons in the solitarius nucleus produce GLP-1 and project to many regions, including the hypothalamus. In the arcuate nucleus of the hypothalamus, which contains GLP-1 receptor, the GLP-1 agonist liraglutide caused activation of pro-opiomelanocortin neurons and inhibition of neuropeptide Y/agouti-related peptide neurons via post-synaptic GABAA receptors, but enhancement of pre-synaptic GABAergic neurons. GLP-1R mRNA expression was also seen in both cultured, embryonic primary cerebral cortical neurons and ventral mesencephalic (dopaminergic) neurons, both of which are vulnerable to hypoxia- and 6-hydroxydopamine-induced cell death, from which GLP-1 conferred protection.

As regards the effect of GLP-1 in AD, it reduced the effects of Aβ and plaque formation in AD model mice, and measures of nutrition, with which GLP-1 is strongly connected, were associated with mortality in patients with AD. That is notable because in a study of 79 patients with AD, 22 died during five years, and being underweight was a major risk factor for that mortality, with a hazard ratio (HR) of 3.34, and poor nutrition had an HR of 5.6.

GLP-1 and Oligodendroglia
Oligodendrocytes, which carry a GLP-1 receptor, have a key role in the myelination of neurons and are decreased in AD. After spinal cord injury, administration of the GLP-1 agonist, exenatide, led to a significant increase in survival of oligodendrocyte progenitor cells, and those pre-oligodendrocytes were decreased in a mouse model of AD.

GLP-1 and Astrocytes
The presence of GLP-1 receptors in astrocytes was demonstrated by Reiner et al., who found that the uptake of a systemically administered fluorophore-tagged GLP-1 agonist exendin-4 was blocked by pretreatment with the competitive GLP-1R antagonist exendin-(9–39). The addition of GLP-1 reduced the declines in glycolysis in astrocytes that had been induced by Aβ, and liraglutide administered to AD patients prevented a decline in glucose metabolism in their brains but did not benefit cognition.

GLP-1 and Microglia
Microglia express receptors for GLP-1, probably accounting for the anti-inflammatory effects of GLP-1 agonists: liraglutide caused significantly decreased levels of IFN-γ, TNF-α, and IL-6; and semaglutide led to reductions in CRP that were positively correlated with reductions in bodyweight, waist circumference, fasting plasma glucose, and fasting serum insulin.

GLP-1, Endothelial Cells, and Pericytes
Endothelial cells (EC) from human coronary arteries expressed the receptor for GLP-1. EECs are among those protected by the inhibition of reactive oxygen species (ROS) that is induced by GLP-1. GLP-1 agonism also induced up-regulation of miR-155 expression in endothelial progenitor cells. The GLP-1 agonist exenatide prevented high-glucose and lipid-induced endothelial dysfunction in cultured human arterioles. Pericytes were also protected by GLP-1 against the toxicity produced by ROS [34]. Pericytes have contractile properties and control the cerebral microvascular flow (CMF). Because the CMF is dysfunctional in AD, its protection by GPL-1 agonists has a potential therapeutic benefit.

If the premise is correct, that addressing all of the affected brain cell types might cure AD or any other neurodegenerative disease, then this article shows that GLP-1 agonists should cure AD, because they address neurons/synapses, oligodendroglia, astroglia, microglia, endothelial cells, and pericytes. However, as a class, GLP-1 agonists fall short of curing AD, so either the premise is incorrect, or there is some other explanation for the failure. It is improbable that the premise is incorrect, since all neurodegenerative diseases result from dysfunction, however generated, of some or all brain cell types [40]. The likeliest explanation comes from data showing that the available GPL-1 agonists have different percentages of either their entry to the brain or in their beneficial effects.

Reference:
https://pmc.ncbi.nlm.nih.gov/articles/PMC11242057/
https://www.medicalnewstoday.com/articles/can-glp-1s-actually-help-treat-alzheimers-latest-trial-data

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Scientists at Northern Arizona University are developing a promising new way to detect Alzheimer’s disease earlier than ever before—by tracking how the brain uses sugar. Using tiny particles in the blood called microvesicles, researchers may soon be able to gather brain-specific information without invasive procedures. If successful, this approach could transform Alzheimer’s diagnosis, monitoring, and even prevention, much like how doctors manage heart disease today.

Researchers at Northern Arizona University (NAU) are testing a new approach that could make it easier for clinicians to spot Alzheimer’s disease sooner and slow its progression.

The project is led by Travis Gibbons, an assistant professor in the Department of Biological Sciences. Supported in part by a grant from the Arizona Alzheimer’s Association, the work focuses on brain metabolism and how the brain uses glucose, the sugar that powers thinking, movement, and emotion.

“The brain is like a muscle,” Gibbons said. “It needs fuel to do work, and its gasoline is blood glucose. A healthy brain is greedy; it burns through glucose fast. But brain metabolism is slower when you have Alzheimer’s. It can be viewed as a canary in the coal mine in the development of the disease.”

Tracking Brain Glucose Metabolism Without Invasive Procedures
Because the brain is difficult to reach, measuring glucose metabolism has historically been tough for researchers. In earlier studies, scientists sometimes inserted catheters into veins in a patient’s neck to collect blood as it left the brain. That kind of invasive sampling is not something that can be done during a routine checkup.

Gibbons and his NAU team are now pursuing a simpler option using commercially available kits designed to isolate and analyze microvesicles circulating in the bloodstream.

“Some of these microvesicles originate in a neuron in your brain, and they’re like messengers carrying cargo,” Gibbons explained. “With these test kits, we can find what kind of cargo is in a microvesicle and run tests on it. It’s been described as a biopsy for the brain, but much less invasive. That’s the appeal of it.”

Microvesicles as a Potential “Biopsy for the Brain”
The method is still being developed, but it could reshape how Alzheimer’s is detected and followed over time. Gibbons said the workflow is demanding and requires careful technique and patience, yet the possible payoff is significant.

In an earlier study, Gibbons and colleagues delivered insulin through the nose, which helps it reach the brain more effectively than standard injections. After that, the team collected blood leaving the brain and identified biomarkers linked to improved neuroplasticity. The group is now trying to find those same biomarkers in microvesicles.

Study Stages From Healthy Volunteers to Alzheimer’s Patients
The research is moving step by step. Gibbons is first validating the approach in healthy participants. Next, he plans to compare findings among people with mild cognitive impairment and people diagnosed with Alzheimer’s to see whether shifts in glucose metabolism can help track how the disease progresses.

“Brain function is notoriously hard to measure, but we’re getting better and better at interrogating brain function through biomarkers,” Gibbons said. “Soon, we might be able to help people protect their brain health and prevent Alzheimer’s disease the same way we protect people from cardiovascular disease by prescribing moderate exercise and a healthy diet. That will help us manage the burden on aging people and society as a whole.”

Gibbons, a member of the Arizona Alzheimer’s Consortium (AAC), is conducting the study with Emily Cope, an NAU associate professor of biological sciences and fellow AAC member; K. Riley Connor, a Ph.D. student in biological sciences at NAU; and Philip Ainslie, a professor at the University of British Columbia’s Centre for Heart, Lung & Vascular Health.

Reference:
https://www.hopkinsmedicine.org/health/treatment-tests-and-therapies/alzheimers-blood-test-detects-early-stages-of-disease

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The FDA’s approval of donanemab (to be marketed under the brand name Kisunla) is a landmark event in the treatment of Alzheimer’s disease. Here is a comprehensive breakdown of what the experts are saying, reflecting the consensus, the hope, and the caution.

The Headline: A New Era of Treatment

The FDA has approved donanemab, a monoclonal antibody therapy, for the treatment of early symptomatic Alzheimer’s disease. This includes patients with mild cognitive impairment (MCI) or mild dementia stages of the disease, who have a confirmed presence of amyloid plaques in the brain.

Donanemab joins lecanemab (Leqembi) as the second drug in its class to be fully approved in the U.S. that changes the underlying course of the disease by clearing amyloid.

What the Experts Are Saying: A Spectrum of Opinions

The expert reaction is broadly positive but nuanced, characterized by “cautious optimism.” Here’s a breakdown of their key points:

1. The Hopeful and Encouraged View: “A Turning Point”

• It validates the Amyloid Hypothesis: For decades, the theory that clearing amyloid-beta plaques could slow Alzheimer’s was just that—a theory. The success of donanemab and lecanemab proves that targeting amyloid is a viable therapeutic strategy. Experts see this as a definitive turning point after many past failures.
• Meaningful Slowing of Decline: In the pivotal clinical trial, donanemab demonstrated a significant slowing of clinical decline by about 35% over 18 months compared to a placebo. For patients and families, this translates to more time to live independently, participate in family events, and manage personal finances.
• A Dosing Endpoint: A unique and patient-friendly feature of donanemab is that treatment can be stopped once a patient’s amyloid plaques are reduced to a very low level. This “treat-to-clear” protocol means patients aren’t necessarily on the drug for life, potentially reducing long-term costs and side effects.

Expert Quote (Representative): “This is the decade where we go from theory to practice. We now have tools that can meaningfully change the trajectory of this disease. It’s not a cure, but it’s the most important breakthrough we’ve ever had.” – Dr. Ronald Petersen, Director of the Mayo Clinic Alzheimer’s Disease Research Center.

2. The Cautious and Pragmatic View: “A Step, Not a Finish Line”

• Significant Risks and Side Effects: The most serious side effects are Amyloid-Related Imaging Abnormalities (ARIA). ARIA can manifest as brain swelling (ARIA-E) or micro-bleeds (ARIA-H). While often asymptomatic and detectable only on MRI, it can be serious and, in rare cases, fatal. Expert consensus is that these risks must be carefully managed.
• Modest Benefit for a High Cost: The 35% slowing is statistically significant, but experts caution that the absolute benefit for an individual patient may feel modest. They weigh this against the very high cost of the drug (Eli Lilly has set a list price of $32,000 per year for donanemab, similar to Leqembi) and the extensive healthcare infrastructure required.
• The Infrastructure Challenge: Administering these drugs is not simple. It requires:
  • Accurate Early Diagnosis: Confirming early Alzheimer’s with PET scans or cerebrospinal fluid tests.
  • Genetic Testing: For ApoE ε4 status, as carriers have a higher risk of ARIA.
  • Specialized Infusion Centers: For monthly IV treatments.
  • Frequent MRI Monitoring: To check for ARIA.
    Many healthcare systems, especially in rural or underserved areas, are not yet equipped for this.

Expert Quote (Representative): “This is a qualified victory. The benefit is real but incremental, and the risks are substantial. The challenge now is to build a system that can deliver these drugs safely, equitably, and only to those who are likely to benefit.” – Dr. Jason Karlawish, Co-Director of the Penn Memory Center.

3. The Future-Oriented View: “A Foundation to Build Upon”

• Combination Therapies are the Future: Experts see donanemab not as the end, but as a foundational treatment. The next logical step is to combine amyloid-clearing drugs with therapies that target tau (the other key Alzheimer’s protein) and drugs that protect nerve cells. Donanemab is the “first piece of the puzzle.”
• Earlier Intervention is Key: The trials show that the earlier you treat, the greater the benefit. This is fueling a massive push for better, cheaper, and more accessible blood tests (e.g., p-tau217) to identify at-risk individuals long before significant symptoms appear.
• Prevention on the Horizon: The ultimate goal is to use these drugs in the pre-symptomatic stage to prevent the disease altogether. Trials are already underway in this direction.

Expert Quote (Representative): “Donanemab is a critical proof-of-concept. It tells us we’re on the right path. Now, we need to build on this success by targeting other aspects of the disease and moving treatment earlier, ultimately aiming for prevention.” – Dr. Reisa Sperling, Director of the Center for Alzheimer Research and Treatment at Brigham and Women’s Hospital.

Connecting Back to the Predictive Tool

This approval makes the predictive tool for Alzheimer’s risk mentioned in the previous article even more relevant.

• Early Identification is Everything: With an effective treatment now available, identifying people at high risk for memory decline before it becomes significant is crucial. The predictive tool (using APOE, MMSE, and subjective complaints) could be a first-line, low-cost method to flag individuals who should then undergo more definitive testing (amyloid PET or blood tests) to see if they are candidates for donanemab.
• A Pathway to Treatment: The workflow becomes: Risk Calculator -> Confirmatory Amyloid Test -> Donanemab Treatment. This creates a proactive pathway from risk assessment to intervention.

Conclusion: A Watershed Moment with Work Ahead

The consensus among experts is clear: The FDA’s approval of donanemab is a watershed moment for the Alzheimer’s field. It provides a new, effective treatment option that meaningfully slows the disease.

However, it comes with significant challenges regarding safety, cost, and healthcare delivery. The excitement is tempered by a sober understanding of the work required to integrate this therapy into real-world practice. For patients and families, it represents a new, tangible hope—a chance to buy more quality time in the early stages of a devastating disease.

Reference:
https://www.fda.gov/drugs/news-events-human-drugs/fda-approves-treatment-adults-alzheimers-disease
https://www.medicalnewstoday.com/articles/fda-approves-alzheimers-drug-donanemab
https://www.alz.org/alzheimers-dementia/treatments/donanemab
https://www.neurologylive.com/view/eli-lilly-anti-amyloid-therapy-donanemab-gains-eu-approval-alzheimer-disease

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The Headline: A New, Accessible Risk Calculator

Researchers have developed a new, relatively simple tool that can estimate an individual’s risk of developing memory and thinking problems related to Alzheimer’s disease in the future. Unlike expensive or invasive tests like PET scans or spinal taps, this tool uses easily obtainable information, making it a potential game-changer for primary care and public health.

The tool is often referred to as a risk stratification model or cognitive impairment risk calculator.

The 3 Key Factors

The predictive power of the tool comes from a combination of three primary factors. While the exact weighting in the algorithm is complex, these are the core elements:

1. A Specific Genetic Marker: APOE-e4 Allele
   • What it is: The APOE gene comes in several forms, and the APOE-e4 variant is the strongest known genetic risk factor for late-onset Alzheimer’s disease.
   • How it’s measured: Through a simple blood or saliva test (like a direct-to-consumer DNA kit). Inheriting one copy of e4 from a parent increases risk; having two copies increases it significantly.
   • Why it matters: This factor provides a baseline biological risk that the other factors can amplify or moderate.
2. A Memory Test Score: The Mini-Mental State Examination (MMSE)
   • What it is: A brief, 30-point questionnaire used extensively in clinical and research settings to screen for cognitive impairment. It tests orientation, memory, attention, and language.
   • How it’s measured: Administered by a healthcare professional in about 10 minutes.
   • Why it matters: It provides a snapshot of current cognitive function. A lower score, even within the “normal” range, can indicate the very earliest, subtle signs of decline.
3. Subjective Memory Complaints
   • What it is: The individual’s own perception that their memory or thinking skills have declined. This isn’t about occasionally misplacing keys, but a persistent, noticeable change confirmed by the person or a close family member.
   • How it’s measured: Through a standardized interview or questionnaire.
   • Why it matters: A person’s subjective experience of their own cognitive decline is a powerful predictor. It often precedes measurable deficits on objective tests and can indicate early brain changes.

How the Tool Was Developed and Works

• The Data Source: Researchers built this model by analyzing data from large, long-term studies of older adults (e.g., the Alzheimer’s Disease Neuroimaging Initiative – ADNI). They tracked thousands of people with normal cognition, noting who developed Mild Cognitive Impairment (MCI) or Alzheimer’s dementia over time.
• The Algorithm: Using machine learning, they identified which combination of factors at the study’s start most accurately predicted who would later develop cognitive problems. The interplay of the genetic risk (APOE-e4), a slightly lower current test score (MMSE), and the presence of subjective complaints proved to be a highly predictive triad.
• The Output: The tool generates a percentage or a risk category (e.g., low, medium, high) for the likelihood of developing memory issues within a specific timeframe, such as the next 2-5 years.

Significance and Potential Benefits

1. Early Identification: It can flag at-risk individuals long before significant symptoms appear, moving towards a model of prevention rather than reaction.
2. Accessibility and Cost-Effectiveness: It uses simple, low-cost measures, making it feasible for use in a primary care doctor’s office.
3. Enrolling the Right People in Clinical Trials: This is a major hurdle. By identifying high-risk individuals, researchers can enroll them in prevention trials for new drugs and therapies, increasing the chances of finding effective treatments.
4. Empowering Lifestyle Changes: A person deemed “high-risk” would have a powerful motivation to adopt brain-healthy behaviors, such as:
   • Managing blood pressure and cholesterol
   • Engaging in regular physical exercise
   • Maintaining a healthy diet (e.g., Mediterranean diet)
   • Staying socially and cognitively active

Important Limitations and Considerations

• It’s a Prediction, Not a Diagnosis: This tool estimates risk, not certainty. A high score does not mean a person will develop Alzheimer’s, and a low score does not guarantee they won’t.
• Focus on a Specific Group: Many of these models were developed and validated in populations of a certain age (often 65+) and specific ethnicities. Their accuracy may vary for younger or more diverse groups.
• Ethical and Psychological Implications: Knowing one’s high genetic and cognitive risk can cause significant anxiety. Any use of this tool must be accompanied by proper counseling to explain the results and their implications.
• It’s a Starting Point: A high-risk score would likely lead to more comprehensive testing with a neurologist to rule out other causes and confirm the findings.

Conclusion

This new predictive tool represents a significant step forward in the fight against Alzheimer’s. By demystifying risk through three key factors—genetics, current cognitive performance, and personal experience—it provides a practical and powerful way to identify vulnerable individuals earlier than ever before. This opens the door to more targeted prevention strategies and more efficient research, ultimately bringing us closer to a future where Alzheimer s-related memory loss can be prevented or significantly delayed.

Reference:
https://www.medicalnewstoday.com/articles/new-tool-predicts-future-alzheimers-memory-risk-age-genetics
https://pmc.ncbi.nlm.nih.gov/articles/PMC11071573/
https://www.sciencedirect.com/science/article/pii/S2274580725002675
https://newsnetwork.mayoclinic.org/discussion/mayo-clinic-scientists-create-tool-to-predict-alzheimers-risk-years-before-symptoms-begin/#

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The Headline in Context: “Daily Calcium Supplements Not Linked to Dementia”

This headline stems from research that aimed to settle a scientific debate. For some time, there was a question mark over whether calcium supplements, widely taken for bone health, could increase the risk of dementia, particularly vascular dementia.

The recent, large-scale studies have largely put that fear to rest, finding no significant link between calcium supplementation and an increased risk of cognitive decline.

Key Details of the Research

The most prominent studies on this topic, often cited in recent news, have characteristics like:

• Large Sample Size: They often involve tens of thousands of participants, which makes the findings more reliable.
• Long Follow-up Period: Researchers track participants for many years (e.g., 5, 10, or even 17 years) to see if dementia develops.
• Focus on Older Adults: The research typically focuses on older populations (both men and women) who are most at risk for both osteoporosis and dementia.
• Distinguishing Between Sources: Many studies carefully differentiate between dietary calcium (from food) and supplemental calcium (from pills).

What the Findings Actually Mean

1. No Causal Link Found: The core finding is that there is no evidence that taking calcium supplements causes dementia. The rate of dementia diagnoses in people who took supplements was not higher than in those who did not.
2. Reassurance for Bone Health: This is good news for the millions of people, especially postmenopausal women, who take calcium (and Vitamin D) on the advice of their doctors to prevent osteoporosis and fractures.
3. It Doesn’t Mean Calcium Prevents Dementia: It’s crucial to note that the study suggests “no link,” not a “protective link.” Calcium supplements are not being promoted as a way to prevent cognitive decline. Their primary benefit remains skeletal health.

Why Was This Ever a Concern?

The initial concern arose from a biological hypothesis. Calcium plays a vital role in the body, but in the wrong place, it can be harmful. The theory was:

• High doses of supplemental calcium could lead to a rapid increase in blood calcium levels.
• This could potentially contribute to the calcification of blood vessels, including those in the brain.
• Vascular calcification is a risk factor for strokes and vascular dementia.

The recent large studies have effectively shown that this theoretical risk does not translate into a measurable increase in dementia cases in the general population.

Important Considerations and Limitations

While the findings are reassuring, it’s important to view them with nuance:

• Follow Your Doctor’s Advice: Do not start or stop any supplement regimen without consulting your healthcare provider. They can assess your individual needs, dietary intake, and risk factors.
• Diet is Still Best: The preferred way to get calcium is through a balanced diet rich in foods like dairy products, leafy greens, and fortified foods. The body generally handles dietary calcium more efficiently.
• Potential for Other Risks: Very high doses of calcium supplements (typically over 2,000-2,500 mg per day from all sources) can still pose other risks, such as kidney stones or constipation. The “sweet spot” is getting the recommended amount for your age and sex, not mega-dosing.
• Vitamin D is Key: Calcium absorption depends heavily on having adequate Vitamin D levels. The two are almost always discussed together for bone health.

Conclusion

In short, the current body of evidence provides strong reassurance that taking daily calcium supplements at recommended doses does not increase your risk of developing dementia. This allows individuals and their doctors to make decisions about bone health based on skeletal needs without undue worry about cognitive side effects.

Disclaimer: This information is for educational purposes only and is not a substitute for professional medical advice. Always talk to your doctor about any health concerns and before making changes to your supplement routine.

Reference:

https://www.medicalnewstoday.com/articles/daily-calcium-supplements-not-linked-to-dementia

https://www.sciencedirect.com/science/article/pii/S2666606525002330

https://www.pharmacytimes.com/view/data-reinforces-that-calcium-supplementation-is-not-linked-to-dementia-risk-in-older-women

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