Gut microbiome shifts may begin before Alzheimer’s symptoms appear

 Then have your competent? doctor test for this so THOSE EXACT PREVENTION PROTOCOLS CAN BE INITIATED! Don't have any, do they? PURE INCOMPETENCE! 

Why you need them;

1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.

2. Then this study came out and seems to have a range from 17-66%. December 2013.`    

3. A 20% chance in this research.   July 2013.

4. Dementia Risk Doubled in Patients Following Stroke September 2018 

Gut microbiome shifts may begin before Alzheimer’s symptoms appear

A new review traces how diet, gut bacteria, and their metabolites may intersect with the silent biological changes that precede cognitive decline.

Want to read later? Download your PDF copy by clicking here.

In a recent narrative review published in the journal Nutrients, researchers across Australia summarized evidence on the gut microbiota, microbial metabolites, and dietary patterns in relation to early Alzheimer’s disease (AD). The review did not generate or analyze new data.

AD has a long preclinical stage when metabolic alterations, amyloid accumulation, and neuroinflammation develop while people remain cognitively unimpaired (CU). Understanding these biological changes can help elucidate mechanisms pertinent to early prevention. Recent findings suggest that early AD pathology may be accompanied by alterations in the gut microbiota and other systemic changes. Diet plays an important role in gut microbiota composition and metabolic output.

Diet-induced changes in the microbiota may influence gut–brain communication relevant to metabolic and neuroinflammatory regulation. Research also links long-term dietary patterns to the risk of cognitive impairment and AD. Nevertheless, the relevance of microbiome–diet interactions to microbial functional pathways in preclinical AD remains poorly defined. In this narrative review, researchers summarized evidence linking the gut microbiota, microbial metabolites, and diet to early AD.

AD: Diagnosis and Therapeutic Context

Research advances have enabled AD detection based on biological markers without relying solely on clinical symptoms. Cerebrospinal fluid (CSF) biomarkers and amyloid positron emission tomography (PET) imaging enable the detection of pathology in CU individuals. Standardized amyloid PET quantification, such as the Centiloid scale, can help stratify people along the preclinical continuum and facilitate comparisons across studies.

Current AD treatments offer limited benefit once cognitive decline is established. Common symptomatic treatments, including memantine, donepezil, galantamine, and rivastigmine, provide modest cognitive and functional improvements. Further, while disease-modifying therapies, for example, lecanemab, have been developed for early-stage AD, they are restricted to select populations and have limited clinical benefit.

As such, most available treatments are initiated only after substantial damage has occurred, thereby reducing their capacity to meaningfully modify disease progression. This therapeutic limitation constitutes a substantial challenge in AD treatment, underscoring the need for further research and attention toward earlier AD stages.

Gut–Brain Communication

The gut–brain axis (GBA) is the bidirectional communication network between the central nervous system (CNS) and the gastrointestinal system. It plays an important role in regulating physiological processes, including brain function, metabolism, and immune activity. Alterations in the microbiota composition can modify metabolic and inflammatory conditions in ways that may increase vulnerability to neurodegenerative processes.

Microbial metabolites are an important component of gut–brain communication. Short-chain fatty acids (SCFAs), the most studied metabolites, regulate immune cell differentiation, metabolic pathways, epithelial barrier integrity, and cytokine production. SCFAs can modulate neuronal function and neuroinflammatory processes through these actions. Emerging evidence suggests that GBA disruptions may contribute to the metabolic and inflammatory disturbances seen in early AD. However, direct human evidence in preclinical AD remains limited, and SCFA effects may depend on their concentration and biological context.

Gut Microbiome Dysregulation in AD

A growing body of research suggests that AD is associated with changes in gut microbiota function and composition. In particular, reduced abundance of SCFA-producing genera, such as Eubacterium, Roseburia, and Faecalibacterium, has been commonly reported in AD and cognitive impairment. Meanwhile, some studies report an increased relative abundance of Escherichia/Shigella and other Proteobacteria, which are associated with inflammatory signaling, metabolic imbalance, and oxidative stress.

Microbiota functional alterations in AD include disruptions in fermentation pathways, changes in lipid and amino acid metabolism, and decreases in SCFA biosynthesis. Early changes in microbial metabolic pathways and SCFA-producing taxa have been reported in a small number of studies involving CU individuals with biomarker evidence of amyloid pathology. Although studies have reported inconsistent findings, they suggest that the earliest stages of AD may be characterized by gut microbial dysregulation.

Dietary Patterns Associated With AD

Dietary Approaches to Stop Hypertension (DASH) and the Mediterranean diet (MD) are associated with improved cognitive, cardiovascular, and metabolic outcomes in aging populations. Both emphasize increased intake of plant-based foods, while limiting processed and red meats, added sugars, and saturated fats. Higher adherence to these diets is linked to reduced cerebral amyloid burden, slower cognitive decline, and improved vascular function in older individuals.

The Mediterranean-DASH Intervention for Neurodegenerative Delay (MIND) diet, which combines elements from DASH and MD, has similarly been associated with slower accumulation of AD-related pathology. Further, the prudent dietary pattern has been associated with improved inflammatory and metabolic profiles in aging populations. It is characterized by high intake of fruits, whole grains, vegetables, fish, low-fat dairy, and legumes. The prudent dietary pattern has been associated with higher microbial diversity and enrichment of SCFA-producing taxa.

Concluding Remarks

Collectively, available research suggests that alterations in the composition and metabolic activity of the gut microbiota may be associated with early AD pathology. Reductions in SCFA-producing taxa and alterations in microbial metabolic pathways have been observed in a limited number of studies involving CU populations with amyloid pathology.

However, the current evidence base has important limitations. Most studies have involved populations with AD or mild cognitive impairment rather than biomarker-confirmed preclinical AD, and much of the available evidence is cross-sectional, preventing conclusions about the direction of the relationship. Sequencing has generally been limited to the genus level, while few studies have jointly assessed diet, gut microbiota, microbial functional pathways, SCFAs, and amyloid pathology. As a narrative review, this work also focused primarily on SCFAs rather than other potentially relevant microbial metabolites.

Future studies should prioritize longitudinal, species-level metagenomic analyses in CU individuals grouped by amyloid status. These studies should assess microbial functional pathways, SCFAs, and diet within the same cohort. Researchers should also investigate fecal microbiota transplantation as a potential intervention in experimental AD models.

Journal reference:

• Dissanayaka DMS, Rainey-Smith SR, Sohrabi HR, et al. (2026). Gut Microbiome Changes in Preclinical Alzheimer’s Disease. Nutrients, 18(15):2469. DOI: 10.3390/nu18152469. https://www.mdpi.com/2072-6643/18/15/2469

Blood Test Accurately Predicts Five-Year Alzheimer’s Risk

 

Is your doctor competent? enough to have this test ready for you; AND  have EXACT DEMENTIA PREVENTION PROTOCOLS READY,  based on your risk of dementia post stroke?

Your risk of dementia, has your doctor told you of this?  Your doctor is responsible for preventing this! Is s/he willing to prevent this?

1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.

2. Then this study came out and seems to have a range from 17-66%. December 2013.`    

3. A 20% chance in this research.   July 2013.

4. Dementia Risk Doubled in Patients Following Stroke September 2018 

The latest here:

Blood Test Accurately Predicts Five-Year Alzheimer’s Risk

Summary: A new study establishes the long-term prognostic power of the blood-based biomarker p-tau217. The analysis reveals that asymptomatic individuals presenting with very high baseline p-tau217 concentrations face an absolute 38% risk of developing cognitive impairment within 5 years, escalating to 78% within 10 years.

This predictive capability operates entirely independent of amyloid PET plaque profiles and APOE4 genetics, providing a validated screening standard to select high-risk candidates for targeted Alzheimer’s disease prevention trials.

Key Facts

• The 5-Year and 10-Year Risk Trajectories: The study successfully converted raw p-tau217 biomarker levels into individual risk forecasts. Cognitively healthy older adults who registered “very high” baseline p-tau217 levels demonstrated a 38% absolute risk of developing cognitive impairment within 5 years. Over a 10-year horizon, that predictive risk escalated dramatically to 78%.
• Total Independence from Other Risk Factors: Crucially, the p-tau217 biomarker predicted future cognitive decline entirely independent of other established risk profiles. Its mathematical accuracy held firm even when accounting for the physical presence of amyloid-beta plaques on PET scans or high-risk genetic variations like the APOE4 allele.
• Current Asymptomatic Clinical Restraint: Despite the high accuracy of the test, Dr. Reisa Sperling emphasizes that currently available blood tests are not recommended for healthy, asymptomatic individuals in everyday clinical practice. Because there are no approved disease-modifying therapies for asymptomatic pre-clinical stages, a positive test cannot alter standard medical options.
• The Clinical Standard Recommendation: For any individual discovering a high-risk profile today, the foundational medical guidance remains strictly behavioral and preventative: regular cardiovascular exercise, a highly nutritious diet, strict sleep prioritization, and aggressive overall metabolic wellness tracking.(DEMAND your doctor PROVIDE EXACT PREVENTION PROTOCOLS! None of this useless guideline crapola! The need has been known for decades! That's a long time to BE COMPLETELY INCOMPETENT!) 
• The “Cholesterol Test” Target: The ultimate goal of the Mass General Brigham team is to mature p-tau217 testing into the neurological equivalent of a standard cardiovascular cholesterol screening, providing an accessible tool that safely guides proactive monitoring and early clinical interventions years before a devastating event occurs.
• Gateway to Clinical Prevention Trials: The primary immediate application for p-tau217 testing is the rapid, low-cost screening of ideal candidates for ongoing disease-modifying therapy clinical trials. By identifying individuals with high risk before symptoms manifest, researchers can test preventive treatments when the brain is most receptive to preservation.

Source: Mass General

A blood test for the biomarker phosphorylated tau 217 (p-tau217) recently received federal clearance, but questions have emerged around the extent to which such tests can accurately predict whether a cognitively healthy individual will go on to develop cognitive impairment—a key symptom of Alzheimer’s disease.

A new, international study involving researchers across three continents and led by experts from the Mass General Brigham Neuroscience Institute sheds new light on the prognostic value of such tests.

The study found that cognitively unimpaired individuals with very high levels of the biomarker had a 38% absolute risk of developing cognitive impairment over the next five years—and higher risk over the next 10 years.

A high baseline p-tau217 blood draw acts as an independent prognostic clock, predicting a 38% absolute risk of clinical cognitive impairment within 5 years and a 78% risk within 10 years. Credit: Neuroscience News

Results are presented at the Alzheimer’s Association International Conference and simultaneously published in JAMA.

“We do not yet have disease-modifying treatments for people who find out they are at high risk for developing cognitive impairment due to Alzheimer’s disease, which is why we don’t recommend currently available blood tests for asymptomatic individuals.

Today, our medical advice would remain the same regardless of test results: exercise regularly, maintain a healthy diet, and prioritize sleep and overall wellness,” said senior and corresponding author Reisa Sperling, MD, a neurologist with the Mass General Brigham Neuroscience Institute.

“But the preventive care landscape could change rapidly if ongoing trials of disease-modifying therapies prove beneficial. In the future, these tests could help identify those who might benefit most from these treatments. Our long-term goal is to get us to where cholesterol testing is in predicting your risk of a heart attack.”

To conduct their study, investigators pooled data from across six observational and clinical trial studies based in North America, Japan, and Australia. The studies included 2,684 cognitively unimpaired older adults. Blood samples were tested for p-tau217 levels and PET imaging was conducted when participants enrolled in the studies to get a baseline reading. Participants received annual follow-ups to assess cognitive function. The earliest enrollment in one of the studies was in 2004, and the most recent follow-up was in 2025.

The research team charted participants’ cognitive trajectories, quantifying their risk of developing cognitive impairment over time. Approximately 478 participants progressed to cognitive impairment. Higher p-tau217 levels at baseline were significantly associated with cognitive impairment. Individuals with very high p-tau217 levels had a 38% risk of developing cognitive impairment over five years. This risk grew with time, reaching 78% over 10 years. However, data were much sparser for 10-year outcomes and beyond.

“This is a critical step toward better understanding what p-tau217 can tell us about a person’s risk for cognitive impairment,” said lead author Rachel F. Buckley, PhD, a cognitive neuroscientist with the Mass General Brigham Neuroscience Institute. “What really sets this work apart is that it estimates an individual’s level of risk for cognitive impairment. We harmonized data across six cohorts, creating a large and varied data set, and still found consistent results showing how p-tau217 informs risk over time.”

Researchers found that the blood test predicted risk independent of other known risk factors, including amyloid-beta plaques that can appear on PET scans and known genetic risk factors (such as APOE4). While the study’s design has many strengths, it is still limited by selection bias and focuses on relatively short-term risks, rather than over a lifetime. Future work is needed to validate the findings in broader and more representative populations. By following participants over longer periods, researchers will be able to further refine individual risk estimates.

One thing in your blood may predict Alzheimer’s risk years before symptoms

 Is your doctor competent? enough to have this test ready for you; AND  have EXACT DEMENTIA PREVENTION PROTOCOLS READY,  based on your risk of dementia post stroke?

Your risk of dementia, has your doctor told you of this?  Your doctor is responsible for preventing this! Is s/he willing to prevent this?

1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.

2. Then this study came out and seems to have a range from 17-66%. December 2013.`    

3. A 20% chance in this research.   July 2013.

4. Dementia Risk Doubled in Patients Following Stroke September 2018 

The latest here:

One thing in your blood may predict Alzheimer’s risk years before symptoms

A blood test that measures a single protein may be able to predict a seemingly healthy person’s risk of developing Alzheimer’s-related cognitive decline up to a decade before any symptoms appear, according to new research.

The findings, presented at the Alzheimer’s Association International Conference (AAIC) 2026 in London, England, found that older adults with very high levels of a biomarker called p-tau217 had roughly a 78 percent chance of developing cognitive impairment within 10 years, even though they showed no signs of memory or thinking problems when tested.

Almost 7 million Americans are living with Alzheimer’s disease today, and that number is projected to nearly double to about 13 million by 2050 if no medical breakthrough changes the trend, according to the Alzheimer’s Association.

‘Tremendous Promise’ but Proceed Carefully

Dr. Manisha Parulekar, co-director of the Center for Memory Loss and Brain Health at Hackensack University Medical Center, New Jersey, told Newsweek the test could transform how doctors approach Alzheimer’s risk.

“A single blood test to detect Alzheimer’s predisposition in cognitively healthy individuals holds tremendous promise,” Parulekar said.

She added that it could move risk assessment “out of specialty clinics and into primary care” and open the door to early, personalized interventions targeting factors such as blood pressure, sleep, hearing and physical activity. It could also speed up recruitment for prevention trials, she said, “enabling us to test whether intervening in the preclinical phase can delay or prevent disease onset.”

psychological distress, anxiety, and anticipatory grief,” and raised concerns about insurance discrimination and unequal access to future care.

“Responsible implementation must pair the test with structured counseling, equitable access to interventions, and robust support infrastructure,” she said.

What the Researchers Found

Researchers had examined blood samples from nearly 2,700 cognitively healthy adults, average age 70, drawn from six major Alzheimer’s research groups and clinical trials. It is among the largest studies of its kind to date. Participants were tracked for an average of nearly five years, with some followed for more than a decade, using standard tests of memory, thinking and daily function.

Adults with p-tau217 levels more than double the study average had an estimated 78 percent risk of cognitive impairment within 10 years, and about a 38 percent risk within five years. Those with moderately elevated levels faced a lower but still notable risk: about 15 percent over five years and 45 percent over 10 years. Notably, the blood test added predictive value beyond what brain scans and genetic testing alone could offer.

P-tau217 is a modified form of the tau protein, which forms tangles in the brain that are a hallmark of Alzheimer’s and are closely tied to cognitive decline. The protein is also linked to levels of amyloid beta, a second hallmark of the disease, making it a useful single marker for both processes.

Study lead author Rachel F. Buckley, associate chair of research at the Mass General Brigham Neuroscience Institute and associate professor of neurology at Harvard Medical School, said in a statement that the results offer “some of the clearest evidence yet that elevated p-tau217 levels may help detect dementia risk years earlier—even in adults with no noticeable memory or thinking problems.”

She said the test could eventually help recruit patients for trials of treatments aimed at preventing cognitive decline.

Researchers stressed that the biomarker alone cannot fully predict an individual’s future risk, since age, genetics, kidney function, obesity and racial and ethnic background can all influence both biomarker levels and dementia risk. They said more diverse study populations and longer follow-up periods are needed to refine long-term risk estimates.

The p-tau217 blood test is FDA-cleared for clinical use in the United States. In May 2025, the U.S. Food and Drug Administration (FDA) cleared the Lumipulse G pTau217/β-Amyloid 1-42 Plasma Ratio, which is manufactured by Fujirebio, as the first in vitro diagnostic blood test to aid in diagnosing Alzheimer’s disease.

Newsweek has reached out to the study’s authors for more information.

Reference

Buckley, R. F., et al. (2026). Prognostic Value of Blood-Based P-Tau217 Levels for Progression to Cognitive Impairment. JAMA. doi:10.1001/jama.2026.12556.

Contact Newsweek editors on this story: Marc Vargas and James Debens

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Blood circRNAs may predict Alzheimer’s before symptoms emerge

 With this your doctor could then implement THOSE EXACT DEMENTIA PROVENTION PROTOCOLS! They incompetently don't exist, do they?

Blood circRNAs may predict Alzheimer’s before symptoms emerge

A blood-based circRNA signature could help identify early Alzheimer’s biology and progression risk, offering a promising new layer beyond amyloid and tau testing.

Study: Blood-based circular RNAs for early diagnosis of Alzheimer’s disease. Image Credit: Andrii Vodolazhskyi / Shutterstock

In a recent study published in the journal Nature Medicine, researchers identified circular ribonucleic acids (circRNAs) in blood with high predictive value for biomarker-confirmed early Alzheimer’s disease (AD) diagnosis. Combining these circRNAs with established markers, such as phosphorylated tau-217 (pTau217), yielded the highest predictive ability. These findings suggest that circRNA investigations could eventually complement blood-based AD biomarker panels to identify people with early AD biology or elevated progression risk. However, the findings need to be validated in larger, diverse prospective clinical cohorts.

AD is the leading cause of dementia. Since pathological alterations in this condition appear before cognitive decline, scientists are developing new strategies to detect AD early and support timely intervention aimed at slowing disease progression. Early identification of the disease before clinical symptoms appear could enable prompt treatment and better clinical planning, and may improve outcomes when paired with effective interventions, while potentially reducing mortality associated with severe disease.

About the study

In the present study, researchers analyzed blood samples of 1,221 participants, including 405 AD patients and 816 cognitively unimpaired adults, using RNA sequencing (RNA-seq). They aimed to identify and validate blood-based circRNAs that could help diagnose AD and monitor disease progression. They used the CircAtlas 3.0 database to examine circRNA expression across 33 tissues and quantitative polymerase chain reaction (qPCR) to assess selected circRNA expression in these tissues.

The team calculated area under the curve (AUC) values to determine the diagnostic utility of a model based on the blood-based circRNAs. They compared the results with blood pTau217 levels to classify biomarker-confirmed AD status. The researchers also replicated the results among 551 participants in the Knight Alzheimer's Disease Research Center (Knight ADRC), including 76 with AD and 475 cognitively unimpaired individuals. They additionally tested the model in the preclinical Anti-Amyloid Treatment in Asymptomatic AD cohort (A4, 1,767 participants), in which almost all participants were cognitively unimpaired at baseline. They used logistic regression models, including the top differentially expressed circRNAs, for statistical analysis.

Among the Knight ADRC participants, the team evaluated the ability of circRNAs and pTau217 biomarkers in blood, and of amyloid-PET status, to predict symptomatic progression. They used Cox regression models to estimate the hazard ratios (HRs) for this analysis.

The team assessed the specificity of blood-based circRNAs for disease detection by comparing findings across other neurodegenerative conditions, including Parkinson’s disease (PD), dementia with Lewy bodies (DLB), and frontotemporal dementia (FTD). They also evaluated whether the overall 34-circRNA model could predict progression of dementia severity using Clinical Dementia Rating (CDR) scores. They also conducted sensitivity analyses stratified by sex, ancestry, and apolipoprotein E4 (APOE4) status. They performed principal component analysis (PCA) to generate covariates for genetic ancestry.

Results

The team identified 34 circRNAs linked to clinical AD status. The overall 34-circRNA prediction signal linearly and consistently increased from the presymptomatic stage around two to four years before symptom onset until symptomatic AD. Most of the identified AD-related circRNAs were highly expressed and showed preferential expression in the brain, although the study could not prove that the blood circRNAs were brain-derived, and their links with clinical AD were observed regardless of their cognate linear messenger RNA counterparts. The overall circRNA model scores were associated with dementia severity and could capture dynamic signals of AD progression that other pathology-focused biomarkers might miss.

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The results were comparable to blood pTau217 levels and also replicated in the A4 and Knight ADRC study groups. The circRNA-based model outperformed blood pTau217 alone for biomarker-confirmed A−T− cognitively unimpaired versus A+T+ AD classification, achieving an AUC of 0.95 compared with 0.88 for blood pTau217 alone. The team achieved the highest AUC by integrating both biomarkers (0.97-0.98). The combined circRNA and pTau217 model helped differentiate non-progressors from high-risk progressors. This could be potentially useful for monitoring AD progression in the era of new AD treatments, especially those targeting amyloid plaques, as circRNAs may indicate broader biological changes and symptom progression beyond amyloid pathology.

The blood-based circRNA model also specifically detected AD-related changes and showed low predictive performance for conditions such as PD, DLB, and FTD. These markers may therefore potentially help stratify progression risk and be explored for monitoring disease biology beyond amyloid pathology. Among Knight ADRC participants, circRNAs (HR, 2.9) outperformed pTau217 (HR, 1.8) and amyloid-PET in predicting progression to the symptomatic stage of AD. The sensitivity analysis yielded similar results, highlighting the robustness of the primary findings. The findings were largely similar for European, African, and mixed populations, supporting potential robustness across ancestries, although some ancestry subgroups were small.

Conclusion

The findings highlight blood-based circRNAs as promising, non-invasive, scalable, and high-precision investigational biomarkers for predicting biomarker-confirmed AD status and symptomatic progression risk. Based on these findings, circRNA detection in blood could one day be used as an adjunct to early AD detection, provided the findings are validated in larger, prospective clinical studies. In the future, researchers should also explore the influence of AD-related comorbidities on blood-based circRNA levels.

The findings are especially relevant since circRNAs are highly stable, tissue-specific, and can be measured in blood. This approach may be clinically useful because traditional AD biomarker assessment has often relied on cerebrospinal fluid (CSF) obtained through lumbar puncture or expensive amyloid PET scans.

Want to read later? Download your PDF copy by clicking here.

The No. 1 Most Important Alzheimer's Disease Symptom a Doctor Monitors in Herself

 FYI.

The No. 1 Most Important Alzheimer's Disease Symptom a Doctor Monitors in Herself

Anyone who’s lost a loved one to Alzheimer's disease may be worried about noticing symptoms in themselves.

Alzheimer's takes a terrible toll. It’s the most common cause of dementia — abnormal brain changes that lead to memory loss, impaired thinking skills and confusion.

Patients become unable to learn, remember and recognize family.

The biggest risk factor is age, followed by family history, says Mary Sano, Ph.D., professor of psychiatry and director of the Alzheimer's Disease Research Center at Mount Sinai School of Medicine in New York.

She’s a neuropsychologist — a specialist who focuses on the brain and behavior. A patient may be referred to a neuropsychologist for an evaluation when they, their family or their doctors notice a change in behavior that could signal dementia.

People with cognitive decline may be unaware of the disease in themselves, a condition known as anosognosia. But they may notice important clues in early stages of brain changes.

“I think everyone as they age is probably attentive to cognitive impairment,” Sano tells TODAY.com.

“A very common thing can be that people really do feel a difference that others aren't aware of or don't acknowledge. I see that very often in participants. They say, ‘I'm just not doing this as well,’ or, ‘I feel foggy when I'm trying to do something.’”

Knowing what she knows, here are the Alzheimer’s disease symptoms she pays attention to in her own life:

Missing Periods of Time

Not being able to figure out: What did I do for breakfast this morning? What routine did I follow this morning?

“That can be a problem,” Sano notes.

Staci Marklin, a 47-year-old Tennessee woman diagnosed with early-onset Alzheimer's disease, says she was “having instances where it felt like things were just gone,” including when her 3-year-old son was born.

“Once someone asked me my son's date of birth, and I had no idea,” Marklin told Buzzfeed.

Hearing Concern from Others

The "most important thing" is being open to hearing a concern from others, since Alzheimer’s disease symptoms are often identified by someone else, Sano says.

“Be open to the fact that someone says, ‘I don't think you're doing this as well as you used to,’” she advises.

Accept it as someone noticing a change that's worthy of getting checked out, she adds.

For example, other people commenting that you’re repeating yourself or asking the same question over and over again might be cause for concern.

Misplacing Things in Odd Places

There are common stories of someone putting their keys in the refrigerator or another inappropriate place, Sano notes.

“My experience is when those things are happening, many more things have happened before that,” she says.

Being More Anxious or Upset

Not being able to find your keys or your phone provokes unusual anxiety.

“Sometimes people can have an awareness of that, and are particularly irritable or anxious around their own performance,” Sano says.

“That might indicate that, in fact, they have this worry about some change that they can't articulate, and it's worthy of conversation with a physician.”

Forgetting to Pay Bills

“That can be a very important sign,” Sano says. “I think that's probably the biggest kind of problem.”

How to Get Help

If you’re worried, talk with a friend, family member or another trusted person in your circle and ask if they’ve also noticed changes.

If any of your symptoms are acknowledged by someone else, it’s worthy of a medical evaluation, Sano advises. Tell your doctor about your concerns.

You can be referred to a neuropsychologist for standardized cognitive testing and more.

“If I have someone whose testing is normal, but they really insist that there's something different, they can then be recommended for biological testing and see if there is evidence of Alzheimer's pathology,” Sano says.

Two blood tests were approved by the U.S. Food and Drug Administration in 2025 to help diagnose or rule out Alzheimer’s disease.

One can be used in a primary care setting and is designed to rule out the presence of amyloid plaques, a hallmark sign of Alzheimer’s disease. The sticky plaques can cause brain cells to die, so checking for amyloid in the brain helps doctors find out whether Alzheimer’s is the potential cause, according to the National Institutes of Health.

The other test is used for early detection of amyloid plaques. Both are for people 55 years old and older who have symptoms of the disease.

Can Alzheimer's Disease Be Prevented?

That's not been shown, but lifestyle factors may play a role in improving cognitive status, Sano says.

“I always say that people should ask themselves: Are they socially and intellectually active? Are they eating a healthy diet? And are they engaging in exercise?” she advises.

These habits are being studied to see if they might give people resilience against diseases that impair cognition, she adds.

This article was originally published on TODAY.com

The No. 1 Most Important Alzheimer's Disease Symptom a Doctor Monitors in Herself

 Instead of having to monitor this post stroke why not have your competent? doctor GIVE YOU EXACT PREVENTION PROTOCOLS? The problem has been known for years and your incompetent? doctor has done nothing to solve that?

Your risk of dementia, has your doctor told you of this?  Your doctor is responsible for preventing this! Is s/he willing to prevent this?

1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.

2. Then this study came out and seems to have a range from 17-66%. December 2013.`    

3. A 20% chance in this research.   July 2013.

4. Dementia Risk Doubled in Patients Following Stroke September 2018 

The latest here: 

The No. 1 Most Important Alzheimer's Disease Symptom a Doctor Monitors in Herself

Anyone who’s lost a loved one to Alzheimer's disease may be worried about noticing symptoms in themselves.

Alzheimer's takes a terrible toll. It’s the most common cause of dementia — abnormal brain changes that lead to memory loss, impaired thinking skills and confusion.

Patients become unable to learn, remember and recognize family.

The biggest risk factor is age, followed by family history, says Mary Sano, Ph.D., professor of psychiatry and director of the Alzheimer's Disease Research Center at Mount Sinai School of Medicine in New York.

She’s a neuropsychologist — a specialist who focuses on the brain and behavior. A patient may be referred to a neuropsychologist for an evaluation when they, their family or their doctors notice a change in behavior that could signal dementia.

People with cognitive decline may be unaware of the disease in themselves, a condition known as anosognosia. But they may notice important clues in early stages of brain changes.

“I think everyone as they age is probably attentive to cognitive impairment,” Sano tells TODAY.com.

“A very common thing can be that people really do feel a difference that others aren't aware of or don't acknowledge. I see that very often in participants. They say, ‘I'm just not doing this as well,’ or, ‘I feel foggy when I'm trying to do something.’”

Knowing what she knows, here are the Alzheimer’s disease symptoms she pays attention to in her own life:

Missing Periods of Time

Not being able to figure out: What did I do for breakfast this morning? What routine did I follow this morning?

“That can be a problem,” Sano notes.

Staci Marklin, a 47-year-old Tennessee woman diagnosed with early-onset Alzheimer's disease, says she was “having instances where it felt like things were just gone,” including when her 3-year-old son was born.

“Once someone asked me my son's date of birth, and I had no idea,” Marklin told Buzzfeed.

Hearing Concern from Others

The "most important thing" is being open to hearing a concern from others, since Alzheimer’s disease symptoms are often identified by someone else, Sano says.

“Be open to the fact that someone says, ‘I don't think you're doing this as well as you used to,’” she advises.

Accept it as someone noticing a change that's worthy of getting checked out, she adds.

For example, other people commenting that you’re repeating yourself or asking the same question over and over again might be cause for concern.

Misplacing Things in Odd Places

There are common stories of someone putting their keys in the refrigerator or another inappropriate place, Sano notes.

“My experience is when those things are happening, many more things have happened before that,” she says.

Being More Anxious or Upset

Not being able to find your keys or your phone provokes unusual anxiety.

“Sometimes people can have an awareness of that, and are particularly irritable or anxious around their own performance,” Sano says.

“That might indicate that, in fact, they have this worry about some change that they can't articulate, and it's worthy of conversation with a physician.”

Forgetting to Pay Bills

“That can be a very important sign,” Sano says. “I think that's probably the biggest kind of problem.”

How to Get Help

If you’re worried, talk with a friend, family member or another trusted person in your circle and ask if they’ve also noticed changes.

If any of your symptoms are acknowledged by someone else, it’s worthy of a medical evaluation, Sano advises. Tell your doctor about your concerns.

You can be referred to a neuropsychologist for standardized cognitive testing and more.

“If I have someone whose testing is normal, but they really insist that there's something different, they can then be recommended for biological testing and see if there is evidence of Alzheimer's pathology,” Sano says.

Two blood tests were approved by the U.S. Food and Drug Administration in 2025 to help diagnose or rule out Alzheimer’s disease.

One can be used in a primary care setting and is designed to rule out the presence of amyloid plaques, a hallmark sign of Alzheimer’s disease. The sticky plaques can cause brain cells to die, so checking for amyloid in the brain helps doctors find out whether Alzheimer’s is the potential cause, according to the National Institutes of Health.

The other test is used for early detection of amyloid plaques. Both are for people 55 years old and older who have symptoms of the disease.

Can Alzheimer's Disease Be Prevented?

That's not been shown, but lifestyle factors may play a role in improving cognitive status, Sano says.

“I always say that people should ask themselves: Are they socially and intellectually active? Are they eating a healthy diet? And are they engaging in exercise?” she advises.

These habits are being studied to see if they might give people resilience against diseases that impair cognition, she adds.

This article was originally published on TODAY.com