The early signs of Alzheimer’s disease begin accumulating in the brain at least seven years before amyloid plaques become detectable with today’s most advanced scanning technology, a finding published September 2, 2026 in a landmark longitudinal brain imaging study highlighted by ScienceDaily that tracked healthy older adults with repeated scans over nearly 20 years and uncovered structural and metabolic brain changes that consistently preceded every subsequent Alzheimer’s diagnosis. For the 55 million people globally living with dementia and the billions more worried about their future brain health, the discovery of early signs of Alzheimer’s disease years before any symptom, or even any visible plaque, represents the most important shift in Alzheimer’s prevention science since the disease was first described.
The finding carries an urgent, hopeful message: Alzheimer’s does not begin with memory loss. It begins with biological processes that start in midlife, in your 40s and 50s, when every intervention documented in BillboardHealth’s 2026 brain health series has its maximum protective impact. You have more time, and more biological leverage, than you realized.
This article is for informational purposes. See your doctor for any cognitive concerns rather than self-diagnosing. Having risk factors does not mean you will develop Alzheimer’s. A positive biomarker test should be discussed with a neurologist or specialist with appropriate psychological support.
The September 2026 Discovery: Early Signs of Alzheimer’s Disease Appear 7 Years Before Plaques
The study tracked healthy older adults with repeated brain imaging over nearly 20 years, the longitudinal cohort design that is the gold standard for identifying pre-symptomatic biomarkers. By following the same individuals from cognitive health through various stages using multiple modalities of advanced brain imaging, the research team identified which brain changes reliably preceded amyloid plaque deposition visible on PET scanning.
The headline finding. Brain changes associated with Alzheimer’s may begin at least seven years before amyloid plaques become detectable with current PET scans.
What was changing in those 7 years:
- Entorhinal cortex thinning, the brain’s primary memory gateway (the first structure where Alzheimer’s tau pathology begins) shows subtle structural thinning, detectable only by repeated high-resolution structural MRI
- Default mode network metabolic reduction, FDG-PET identifies reduced glucose metabolism in the posterior cingulate cortex, precuneus, and lateral parietal regions years before any amyloid is visible
- Hippocampal volume changes, subtle decreases in the brain’s primary memory-formation center
- White matter microstructure disruption, diffusion tensor imaging detects early damage in the cingulate fasciculus and uncinate fasciculus, white matter tracts connecting memory regions
All of these changes occurred in people who were cognitively normal, passing all standard cognitive tests with scores in the normal range. No behavioral symptom detected them.
The extended Alzheimer’s timeline, what this means.
| Phase | Timing Before Diagnosis | What’s Happening | Detection Method |
| Pre-amyloid brain changes (NEW) | 17–22+ years | Entorhinal thinning, metabolic reduction, white matter changes | Repeated MRI/FDG-PET only |
| Amyloid accumulation | 10–15 years | Plaques form; no symptoms | Amyloid PET, CSF, blood biomarkers |
| Tau spread and synaptic loss | 7–12 years | Tau tangles propagate; still no symptoms | Tau PET, blood p-tau217 |
| Subjective cognitive decline | 2–5 years | Person notices changes; tests still normal | Self-report only |
| Mild cognitive impairment | 1–3 years | Tests confirm objective impairment | Neuropsychological testing |
| Alzheimer’s diagnosis | 0 | Clinical criteria met | Clinical + biomarker |
The prevention implication. If this pre-amyloid window occurs approximately in the mid-40s to mid-50s for most people who develop late-onset Alzheimer’s, the most powerful intervention point in the entire Alzheimer’s disease continuum corresponds to the decade that most people consider their healthiest and most cognitively secure. The time to act is not when you notice memory changes. It is now.
Study limitations. This is an observational longitudinal study, it cannot prove the pre-amyloid brain changes directly cause Alzheimer’s, only that they reliably precede it. The study population of “healthy older adults” may skew toward higher baseline health than the general population. Some people with early biomarker changes never progress to dementia, having these early brain changes does not mean Alzheimer’s is inevitable.
What Are the Early Signs of Alzheimer’s Disease in the Brain Before Symptoms Appear?
The most important insight from the 2026 study: the earliest signs of Alzheimer’s are invisible to the person experiencing them. They are structural and metabolic changes visible only on advanced repeated brain imaging, not behavioral symptoms that someone could notice in themselves or a loved one.
The complete pre-symptomatic Alzheimer’s staging:
Stage A — Pre-Amyloid Changes (NEW — 7+ Years Before Stage B)
The September 2026 discovery. Entorhinal cortex thinning, default mode network metabolic change, white matter microstructure disruption, occurring in cognitively normal people approximately 7 years before the first amyloid plaque becomes PET-detectable. No clinical symptoms. Detectable only by repeated advanced imaging or, potentially in the future, by next-generation blood biomarkers.
Stage B — Amyloid Accumulation (10–15 Years Before Symptoms)
Amyloid plaques begin accumulating. Now detectable by amyloid PET scan, cerebrospinal fluid (CSF) biomarkers, or blood-based biomarkers (plasma p-tau217, Abeta42/40 ratio). This is “preclinical Alzheimer’s”, the person has biological Alzheimer’s pathology but no cognitive symptoms. Approximately 20–30% of cognitively normal 60-year-olds are in this stage.
Stage C — Tau Spread and Synaptic Loss (7–12 Years Before Symptoms)
Tau tangles propagate from the entorhinal cortex into the hippocampus and broader cortical regions via neural circuit connections, the Braak staging sequence known since the 1990s but now placed within the extended pre-amyloid timeline. Synaptic loss begins, the earliest functional change, but cognitive tests remain normal in most people. “Prodromal Alzheimer’s” in the most affected.
Stage D — Subjective Cognitive Decline (2–5 Years Before Diagnosis)
The first symptomatic stage: the individual notices memory or thinking changes that are not yet measurable on standard cognitive tests. They feel “not quite right”, slightly more forgetful, slightly slower to process. Tests are still normal, but the subjective experience is real and meaningful. This stage is increasingly recognized as clinically important: adults reporting subjective cognitive decline have meaningfully higher rates of subsequent MCI and dementia than those who don’t report it.
Stage E — Mild Cognitive Impairment (1–3 Years Before Diagnosis)
Standard cognitive testing (MoCA, MMSE, neuropsychological battery) now confirms objective impairment below age-expected norms, in memory, attention, or executive function. Daily life is still relatively intact. The Emory vitamin D study specifically targeted this MCI population, finding 13% higher cognitive test scores with 5,000 IU vitamin D, intervening at Stage E.
Stage F — Alzheimer’s Disease Diagnosis
Cognitive impairment has progressed to affect daily independence. Clinical and biomarker criteria are met.
Who Is Most at Risk for Pre-Amyloid Brain Changes, and at What Age?
Genetic risk factors:
APOE ε4 carriers, the most important genetic risk factor. Approximately 25% of the population carries at least one APOE ε4 allele; homozygous carriers (ε4/ε4) face 8–12× higher lifetime Alzheimer’s risk. The Stanford brain inflammation research identified APOE ε4 as the gene that impairs LDL clearance and simultaneously makes the aging brain more vulnerable to peripheral immune cell infiltration, now connected to the pre-amyloid window’s entorhinal neuroinflammation. For ε4/ε4 carriers, the pre-amyloid window may begin in the late 30s to early 40s.
First-degree relative with Alzheimer’s. Doubles lifetime risk independent of APOE status.
Down syndrome. The amyloid precursor protein (APP) gene on chromosome 21 means virtually all people with Down syndrome develop Alzheimer’s pathology by their 40s, the most severe genetic loading.
Lifestyle risk factors that accelerate the pre-amyloid phase:
| Risk Factor | Mechanism | BillboardHealth Article |
| Chronic poor sleep | Impaired glymphatic amyloid clearance | Deep Sleep Benefits |
| Indoor PM2.5 | Neuroinflammation, microglial activation | HEPA Filter Study |
| Visceral obesity | Ceramide → amyloid cascade | Belly Fat Article |
| Chronic psychological stress | Cortisol → hippocampal atrophy | Mindfulness Heart Health |
| Sedentary behavior + TV | Hippocampal shrinkage | Sedentary Lifestyle Study |
| Depression | Hippocampal neurogenesis failure | Columbia Depression Study |
| Gut dysbiosis | LPS-driven peripheral immune activation | Gut Health & Memory |
| Vitamin D deficiency | NF-κB neuroinflammation | Vitamin D Cognition |
| B12 deficiency | White matter lesion formation | B12 Deficiency |
| Glucosamine use | Hexosamine neuroinflammation | Glucosamine Alzheimer’s |
The age-specific risk window:
- 40s: When pre-amyloid brain changes may first become detectable in higher-risk individuals. The most impactful prevention decade, all lifestyle interventions have maximum years of accumulated benefit ahead.
- 50s: The midlife brain immune shift peaks (Stanford 2026 study). The hippocampal microglial inflammatory remodeling begins (UC San Diego Science 2026). Amyloid accumulation is beginning in the highest-risk individuals. Critical reinforcement decade.
- 60s: Approximately 20–30% of cognitively normal 60-year-olds have detectable amyloid accumulation. Biomarker testing becomes most clinically meaningful. Lifestyle interventions shift from prevention initiation to progression delay.
- 70s+: Prevention efforts focus on delaying progression. Lifestyle interventions still produce measurable benefit, exercise remains the strongest documented late-stage neuroprotective intervention.
The Alzheimer’s Biomarker Revolution, Can You Detect Early Signs Today?
Blood-based biomarkers, most accessible in 2026:
Plasma p-tau217. The most sensitive single blood marker for Alzheimer’s pathology, a phosphorylated tau protein fragment whose concentration in blood reflects the tau accumulation beginning in the entorhinal cortex. Sensitivity and specificity for amyloid PET positivity now exceeds 90% in research settings. Blood tests for Alzheimer’s are becoming nearly as accurate as spinal fluid tests or PET brain scans. Available from specialist clinics and some direct-to-consumer providers in 2026 at approximately $200–$500. Medicare coverage for primary care screening is expected in 2027–2028.
Plasma Abeta42/40 ratio. Detects the imbalance between amyloid protein subtypes that indicates plaque formation, a lower ratio signals higher amyloid burden. Particularly sensitive for Stage B (amyloid accumulation phase) detection.
Plasma GFAP (glial fibrillary acidic protein). Elevated when astrocytes are activated by neuroinflammation, a marker that appears before amyloid becomes detectable and may reflect the Stage A (pre-amyloid) neuroinflammation documented in the September 2026 study.
Advanced imaging, most definitive, least accessible:
- Amyloid PET scan: gold standard for Stage B detection; $3,000–$5,000; limited insurance coverage for asymptomatic individuals
- Tau PET scan: maps tau tangle propagation stage by stage; even more expensive
- FDG-PET: detects metabolic changes (the Stage A finding); more widely available and partially covered for symptomatic evaluation
What to ask your doctor:
- “Given my family history and APOE status, should I consider blood-based Alzheimer’s biomarker testing?”
- “What plasma p-tau217 or Abeta42/40 testing is available through your practice or referral network?”
- “If I test positive for early biomarkers, what specific lifestyle interventions should I prioritize and in what order?”
The critical caveat. Biomarker testing for cognitively normal people has significant psychological implications. A positive test does not mean you will develop Alzheimer’s, many people with early biomarker changes never progress. Discuss the emotional implications with your doctor before testing, and ensure access to genetic counseling and psychological support if results indicate elevated risk.
Early Signs of Alzheimer’s Disease Prevention: The 7-Year Window That Could Change Everything
Understanding the early signs of Alzheimer’s disease at the biological level, before any memory symptom appears, requires a complete revision of how most people think about dementia prevention timing. The 7-year pre-amyloid window is not just a detection milestone; it is the most powerful intervention window in the entire Alzheimer’s disease continuum, when the protein aggregation that seeds plaque formation can potentially be prevented rather than treated.
Priority 1 — Optimize Glymphatic Amyloid Clearance Through Deep Sleep
The UC Berkeley deep sleep research documented that glymphatic clearance of amyloid and tau occurs primarily during slow-wave sleep, when brain cells shrink, expanding the interstitial space that cerebrospinal fluid flushes clean. This process nightly removes the precursor proteins whose aggregation seeds Alzheimer’s pathology. In the pre-amyloid window, maximizing glymphatic efficiency is the most mechanistically specific intervention available.
Target protocol: consistent bedtime within 30 minutes every night; bedroom 65–68°F/18–20°C; no alcohol after dinner (alcohol dramatically suppresses slow-wave sleep); magnesium glycinate 200–400mg 30 minutes before bed (improves deep sleep architecture); treat sleep apnea if present (the single highest-impact sleep intervention for Alzheimer’s prevention, CPAP therapy dramatically restores glymphatic efficiency).
Priority 2 — Suppress Neuroinflammation
The Stanford and UC San Diego 2026 studies documented that the midlife immune cell brain infiltration (beginning in the 40s) and hippocampal microglial inflammatory remodeling (beginning at 50) precisely overlap with the 7-year pre-amyloid window. Reducing neuroinflammation through multiple complementary pathways:
- Anti-inflammatory dietary pattern: Mediterranean eating reduces NF-κB, IL-6, and TNF-α, the same inflammatory cytokines driving the pre-amyloid neuroinflammatory cascade. The plant-based diet JAMA 2026 study documented simultaneous gut microbiome improvement that reduces LPS-driven peripheral immune activation.
- HEPA air filtration: PM2.5 from indoor air activates exactly the peripheral immune cells and microglia involved in the pre-amyloid neuroinflammatory cascade, as documented in the University of Colorado HEPA study. Running a HEPA purifier in the bedroom during sleep addresses both neuroinflammation reduction and glymphatic optimization simultaneously.
- Gut microbiome health: Gut dysbiosis produces LPS that crosses a permeable gut barrier into the bloodstream, activating peripheral immune cells that infiltrate the aging brain, the exact mechanism the Stanford study documented. The medication-gut microbiome research and artificial sweetener study document the most common gut disruptors to eliminate.
Priority 3 — Exercise for Hippocampal Neurogenesis and BDNF
Exercise is the single most potent stimulus for hippocampal neurogenesis, protecting precisely the brain structure whose thinning the 2026 study identifies as the earliest pre-amyloid change. The Harvard 147,000-person strength training study’s 27% lower neurological disease mortality is mechanistically explained by BDNF-mediated hippocampal protection during the pre-amyloid window.
Target protocol: 90–120 minutes strength training weekly (highest BDNF induction) + once-weekly interval walking (cardiovascular fitness protecting blood-brain barrier integrity) + daily stair climbing (cumulative daily anti-inflammatory and cardiovascular benefit).
Priority 4 — Get the Shingles Vaccine (Shingrix)
The Brown University/Oxford 500,000-person study found 24% lower dementia risk from Shingrix vaccination, the strongest single-decision Alzheimer’s prevention action available. VZV reactivation triggers neuroinflammation that accelerates the peripheral immune cell brain infiltration and microglial inflammatory remodeling occurring in the 7-year pre-amyloid window. Preventing it through vaccination at age 50 (the recommended starting age) addresses the exact biological mechanism the September 2026 study’s pre-amyloid window documents.
Priority 5 — Optimize the Brain-Protecting Vitamin Trio
All three vitamins in BillboardHealth’s 2026 vitamin-brain trilogy directly protect the structures showing pre-amyloid changes:
- Vitamin D: suppresses NF-κB neuroinflammation in microglia; promotes BDNF transcription in hippocampal neurons. Deficiency removes the anti-inflammatory brake from the exact microglial cells most involved in the pre-amyloid neuroinflammatory cascade.
- Vitamin B12: maintains white matter integrity in the memory-connecting tracts disrupted in the pre-amyloid phase. White matter lesion accumulation from B12 deficiency occurs in the same tracts the September 2026 study documents as early Alzheimer’s markers.
- Vitamin C: antioxidant protection of the entorhinal cortex and hippocampus, the first structures affected in pre-amyloid Alzheimer’s, against reactive oxygen species generated by activated microglia.
Priority 6 — Mindfulness and Stress Reduction
Chronic cortisol suppresses hippocampal neurogenesis and accelerates the entorhinal cortical thinning identified as the earliest Alzheimer’s brain change. The September 2026 mindfulness review documented that 8 weeks of daily mindfulness practice reduces cortisol, hs-CRP, and blood pressure, directly addressing the stress-cortisol-neuroinflammation pathway contributing to pre-amyloid accumulation.
Priority 7 — Consider Spermidine
The Oxford Aging Cell RCT on spermidine documented that spermidine activates autophagy, the cellular recycling process that clears damaged proteins and dysfunctional organelles. In the pre-amyloid window, autophagy-activated clearance of misfolded proteins may prevent the protein aggregation that seeds amyloid plaque formation. Wheat germ (2 tablespoons daily), aged cheese, and mushrooms provide meaningful dietary spermidine.
Priority 8 — Coffee
Morning coffee’s NR4A1 anti-inflammatory receptor activation provides direct anti-neuroinflammatory benefit through a mechanism distinct from other dietary interventions, and multiple large observational studies associate regular coffee consumption with 20–30% lower Alzheimer’s risk. Black coffee without sugar or artificial sweeteners maximizes this benefit.
The BillboardHealth Alzheimer’s Prevention Hub, Your Age-Specific Action Plan
If you are in your 40s, The Pre-Amyloid Window Is Open Right Now
The September 2026 finding means your 40s are the most critical Alzheimer’s prevention decade, the window when the biological processes the study documented are beginning in the highest-risk individuals, and when every lifestyle intervention has the maximum years of accumulated benefit ahead. Establish the full protocol this month: sleep optimization as your highest priority (the most mechanistically specific pre-amyloid intervention), followed by regular strength training and aerobic exercise, Mediterranean dietary pattern, HEPA bedroom filtration, gut health protection (eliminate artificial sweeteners, manage medications’ gut effects), and vitamin D, B12, and C adequacy testing.
If you are in your 50s — Reinforcement and Early Detection
The Stanford midlife immune shift peaks in your 50s simultaneously with the hippocampal microglial remodeling. Reinforce all lifestyle interventions established in your 40s. New additions for your 50s: get Shingrix vaccination (the single most evidence-backed prevention decision for this decade), check vitamin D and B12 blood levels and correct deficiencies, consider blood-based Alzheimer’s biomarker testing if you have significant family history or APOE ε4 status, and reduce TV watching and sedentary time (the ARIC study showed hippocampal damage from high TV viewing directly in the age window when the September 2026 study’s pre-amyloid changes are occurring).
If you are in your 60s — Monitoring and Maximum Protection
Add formal cognitive assessment (MoCA with your GP annually), consider amyloid biomarker testing if family history is strong, maximize all lifestyle interventions, treat sleep apnea aggressively if present (CPAP is the single highest-impact late-window intervention for many adults), and maintain social engagement actively, social isolation increases dementia risk by 29% through inflammatory and cognitive reserve pathways.
If you are in your 70s+ — Delay and Quality of Life
Lifestyle interventions produce measurable benefit even in the amyloid-accumulation phase. Prioritize: exercise (strongest late-stage neuroprotective intervention, even stair climbing daily helps), sleep quality, social connection, and cognitive engagement. Ask your neurologist about lecanemab or donanemab eligibility if early amyloid biomarkers are positive, these anti-amyloid drugs show the greatest benefit when started early.
The Most Common Memory Concerns — What They Actually Mean
The pre-amyloid brain changes documented in the September 2026 study are detectable ONLY by repeated advanced brain imaging, not by self-observation of behavioral symptoms. The following guide helps distinguish concerning from reassuring, but a doctor’s assessment is the only accurate determination.
Reassuring — almost always benign:
- Walking into a room and forgetting why (universal, not disease-specific)
- Occasionally forgetting a word but remembering it later
- Being distracted and missing details when multitasking or stressed
- Age-appropriate slowing in processing speed
Worth discussing with your GP (book an appointment within 4–6 weeks):
- Forgetting recent conversations or events more frequently than previously
- Difficulty recalling names of people you know well, consistently, not occasionally
- Getting lost in familiar places or routes
- Increased difficulty with financial management, planning, or complex organization
- Personality or mood changes noticed by family or colleagues
Seek medical attention this week:
- Rapid cognitive change over days to weeks
- Confusion about the current date, year, or location
- Not recognizing close family members or long-time friends
- Any significant cognitive change in a person under 60 (early-onset Alzheimer’s warrants prompt specialist evaluation)
Biomarker tests to discuss with your doctor:
At any age with family history or cognitive concerns, request at your next GP appointment:
- Serum 25-OH-D (vitamin D) and holotranscobalamin (active B12), the two most actionable nutritional brain health tests
- Consider plasma p-tau217 testing (blood-based Alzheimer’s biomarker) if family history or strong risk factors are present
- Mention the September 2026 study: “I’ve read about the 7-year pre-amyloid window study, given my family history, when should I discuss biomarker testing with a specialist?”
The Future of Early Alzheimer’s Detection
Blood-based biomarker testing (p-tau217, plasma Abeta) is expected to receive Medicare coverage for primary care screening in 2027–2028, making preclinical Alzheimer’s detection accessible to all older adults for the first time.
AI-based retinal scanning is advancing rapidly, Alzheimer’s-related amyloid deposits appear in the retina years before cognitive symptoms, and AI analysis of standard retinal photographs may enable mass screening at optometry appointments within 2–3 years.
Digital cognitive biomarkers, smartphone-based typing speed analysis, voice pattern recognition, and gait analysis, are being validated as early cognitive decline detectors accessible to anyone with a modern smartphone.
Lecanemab (Leqembi) and donanemab, FDA-approved anti-amyloid drugs showing efficacy in early Alzheimer’s, will be most impactful when started in the Stage B (early amyloid accumulation) phase, which the September 2026 study’s 7-year extension of the detection window now makes more accessible.
FAQs About Early Signs of Alzheimer’s Disease
What are the earliest signs of Alzheimer’s disease before memory loss begins? The September 2026 study found the earliest signs are invisible, structural brain changes detectable only by repeated advanced imaging: entorhinal cortex thinning, default mode network metabolic reduction, hippocampal volume changes, and white matter microstructure disruption. All occurring 7+ years before amyloid plaques form and 17–22+ years before diagnosis. No behavioral symptom reliably maps to this earliest stage.
How early can Alzheimer’s be detected before symptoms? With current blood tests (plasma p-tau217, Abeta42/40), approximately 10–15 years before symptoms. The September 2026 study extends the known biological timeline by 7 additional pre-amyloid years, total pre-symptom timeline: potentially 17–22+ years. Blood-based testing is available now for $200–$500 through specialist clinics; Medicare coverage is expected in 2027–2028.
What brain changes happen 7 years before Alzheimer’s plaques? Entorhinal cortex thinning, FDG-PET metabolic changes in the default mode network, hippocampal volume reduction, and white matter tract microstructure disruption, all in cognitively normal individuals, detectable only by repeated advanced imaging.
Can blood tests detect Alzheimer’s early? Yes, plasma p-tau217 and Abeta42/40 ratio now exceed 90% sensitivity/specificity for amyloid PET positivity in research settings. Available at $200–$500 from specialist clinics. Medicare coverage expected 2027–2028.
What does the entorhinal cortex do and why does it matter? It is the primary memory gateway between hippocampus and cortex, and the anatomical origin of Alzheimer’s tau pathology (Braak stages I–II). Its thinning in the 2026 study is the earliest structural Alzheimer’s change, making it the primary prevention target.
If my parent had Alzheimer’s, when should I start prevention? Immediately. Given the 17–22+ year biological timeline, if your parent was diagnosed at 75, you may be entering the pre-amyloid window in your early 50s. APOE ε4 carriers may begin earlier. All lifestyle interventions are beneficial regardless of genetic status.
Can lifestyle changes really prevent Alzheimer’s? No intervention guarantees prevention, but the Lancet Commission estimates 45% of dementia cases may be preventable or significantly delayable through modifiable risk factors. The 7-year pre-amyloid window provides the most specific and actionable prevention target yet identified.
What is the difference between normal memory lapses and early Alzheimer’s? Normal: forgetting why you entered a room, occasional word retrieval delay, misplacing objects temporarily, retrieval difficulty, not storage failure. Early Alzheimer’s concern: consistently forgetting recent conversations, repeated questions within short periods, getting lost in familiar routes, difficulty with previously manageable tasks, storage difficulty, not just retrieval delay.
Should I get an APOE genetic test? A personal decision with psychological implications requiring medical guidance. Arguments for: identifies highest-risk group for most urgent action. Arguments against: does not determine destiny; can cause anxiety requiring support. Ensure genetic counseling is available if you test positive.
What is the most important lifestyle change for Alzheimer’s prevention in your 40s? Sleep optimization (enabling maximum glymphatic amyloid clearance) and regular vigorous exercise (BDNF hippocampal protection and neurogenesis). Both address the pre-amyloid biology the September 2026 study documented, and both have decades of compounding benefit ahead when started in the 40s.
This article is for informational purposes. Seek medical evaluation for any cognitive concerns. Having early biomarkers does not mean Alzheimer’s is inevitable, many people with early markers never progress. Biomarker testing should be conducted with appropriate psychological support and specialist guidance.
