Visual Variant of Alzheimer’s Disease (VVAD)

Visual Variant of Alzheimer’s Disease is a form of Alzheimer’s that mainly damages the back parts of the brain (the occipital, parietal, and occipito-temporal lobes). These areas process vision. Because of that, the first problems are with seeing and understanding what you see—for example, finding objects on a crowded shelf, reading, judging distance, or moving safely through a room—even when the eyes themselves are healthy. Memory can be relatively better early on, but visual and spatial problems are strong and gradually worsen over time, like other types of Alzheimer’s. Clinicians often call this syndrome posterior cortical atrophy (PCA), which is most often due to Alzheimer’s disease pathology. NCBIAlzheimer’s JournalsThe Lancet

Visual Variant of Alzheimer’s Disease (VVAD)—often called Posterior Cortical Atrophy (PCA)—is a brain condition where vision problems are the first and main symptoms, not memory loss. The eyes themselves are usually healthy. The problem sits behind the eyes, in the back parts of the brain (the posterior cortex: occipital, parietal, and occipito-temporal lobes) that handle seeing, recognizing, reading, judging distance, and guiding the hands and eyes together. Over time, the disease can spread and cause more typical Alzheimer-type symptoms, but early on the visual thinking system is hit hardest.

In most people, the underlying biology is the same as Alzheimer’s disease: abnormal proteins—amyloid-beta and tau—build up and damage nerve cells and their connections. In VVAD/PCA, this damage is uneven, with extra stress on the visual networks. Because the damage is focused in these regions, people struggle with reading, recognizing objects or faces, judging space, and coordinating eye–hand movements, even though their eye exam may look normal. This mismatch often leads to years of misdiagnosis (e.g., “eye problems,” “anxiety,” or “functional issues”) before the correct answer is found.

Think of vision as three layers working together:

1. Seeing clear details (the eyes and early visual cortex).

2. Understanding what you see (object recognition, words, faces).

3. Using what you see (guiding your hands, finding your way, judging distance and direction).

VVAD targets layers 2 and 3 first. That is why glasses do not fix the problem, and why visual issues can be confusing, variable, and task-specific.

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Types

You will hear clinicians use overlapping systems to describe “type.” The goal is to show which visual stream is most affected, which disease is underneath, and how far along it is.

1) By the visual network involved

• Dorsal (“where/how”)–predominant type.
  Trouble with space and action. People misjudge distance, bump into things, get lost in familiar places, struggle to reach for objects (the hand misses), or cannot scan a page smoothly. Classic features include Balint syndrome (three problems together: simultanagnosia—seeing one piece but not the whole scene; optic ataxia—misreaching; ocular apraxia—trouble starting eye movements).
  Plain language: the brain knows there is something out there but cannot map it correctly or aim at it.

• Ventral (“what”)–predominant type.
  Trouble with recognition. People can see shapes and colors but cannot name or recognize objects, faces (prosopagnosia), or words (alexia).
  Plain language: the image is seen, but the brain does not label it.

• Mixed dorsal–ventral type.
  Many people have a blend of both pathways affected, with problems in spatial skills and recognition.

2) By underlying disease (molecular pathology)

• PCA due to Alzheimer’s disease (most common).
  Same proteins as typical Alzheimer’s, but with a posterior-first pattern.

• PCA due to Lewy body disease (less common).
  Often has visual hallucinations, fluctuations in attention, REM sleep behavior disorder, and sensitivity to antipsychotics.

• PCA due to corticobasal degeneration or other tauopathies (rare).
  May add limb apraxia, stiffness, jerky movements.

• Other rare causes (very uncommon).
  Prion disease or mixed pathologies can rarely mimic PCA.

3) By stage

• Prodromal/posterior MCI stage.
  Mild but specific visual–cognitive problems with everyday tasks, relatively preserved memory and independence.

• Established VVAD/PCA stage.
  Clear everyday disability from visual-processing problems; work, driving, and reading are often affected.

• Advanced stage.
  Wider spread of symptoms, including memory and language problems, with increasing care needs.

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Causes

Note: in medicine, “cause” can mean the disease process driving the problem and also the risk factors that raise the chance of developing it. For VVAD/PCA, the main cause is usually Alzheimer-type pathology in the posterior cortex; the rest are contributors or less-common alternative diseases.

1. Alzheimer-type protein build-up in the posterior cortex.
   Extra tau tangles and amyloid plaques hit the visual networks first, damaging how vision is processed.

2. Uneven (posterior-dominant) spread of tau.
   In VVAD, tau builds more in parietal/occipital regions, explaining the early visual symptoms.

3. APOE-ε4 genetic risk.
   This common gene variant raises overall Alzheimer risk and is also seen in many with PCA; it doesn’t guarantee disease but increases vulnerability.

4. Rare familial Alzheimer mutations (PSEN1, APP, PSEN2).
   Uncommon inherited mutations can produce an early-onset, posterior-heavy Alzheimer picture.

5. Lewy body disease pathology (alpha-synuclein).
   An alternative cause that can present with visual symptoms first, especially hallucinations and attention fluctuations.

6. Corticobasal degeneration (4-repeat tauopathy).
   Rarely, this tau disease focuses on posterior networks, mixing visual and movement/apraxia problems.

7. Mixed pathologies in older adults.
   Some people have a combination (Alzheimer + Lewy or vascular changes), which tilts the picture toward VVAD.

8. Age (most often mid-to-late life).
   VVAD often begins in the 50s–60s, earlier than typical amnestic Alzheimer’s, though later presentations occur.

9. Vascular risk (hypertension, diabetes, high cholesterol).
   These do not “cause” VVAD directly but may lower brain reserve and accelerate decline.

10. Traumatic brain injury (history of significant head trauma).
    Past head injury may reduce brain resilience and raise the chance of neurodegeneration.

11. Poor sleep and sleep apnea.
    Long-term sleep problems and untreated apnea stress brain clearance systems and can worsen cognitive decline.

12. Chronic stress and depression.
    Mood disorders and stress hormones may worsen symptoms and reduce coping, although they are not primary causes.

13. Low cognitive reserve (fewer lifelong learning opportunities).
    Lower reserve can make symptoms appear earlier for the same biological burden.

14. Hearing or vision impairments (sensory deprivation).
    Separate eye or ear problems strain thinking networks and may unmask or magnify VVAD symptoms.

15. Autoimmune/paraneoplastic processes (rare mimics).
    Inflammation or immune reactions can produce look-alike posterior syndromes; these are important to rule out.

16. Prion disease (very rare and much faster).
    Rapidly progressive visual-cognitive decline must be considered when the course is weeks to months rather than years.

17. Environmental toxins (rare, unproven links).
    Severe toxin exposures can injure the brain; firm links to PCA are limited but are considered in unusual cases.

18. Metabolic or nutritional deficiencies (B12, thyroid).
    These do not cause VVAD but can worsen visual cognition and are treatable contributors.

19. Migraine with aura (co-existing visual phenomena).
    Not a cause of VVAD, but can confuse the picture with transient visual distortions.

20. Family history of early-onset or atypical Alzheimer’s.
    A family pattern suggests a genetic contribution, especially when symptoms begin before age 65.

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Symptoms

1. Reading difficulty (alexia-like).
   Words blur or “swim,” lines are lost, or letters seem jumbled despite normal eye exams. Reading speed drops sharply.

2. Trouble recognizing objects.
   Everyday items look unfamiliar or require touch to identify. People may describe “I see it but don’t know what it is.”

3. Face recognition problems (prosopagnosia).
   Familiar people look unfamiliar, leading to social anxiety and misunderstandings.

4. Simultanagnosia (seeing parts, not the whole).
   Someone can spot a single item but struggles to see a whole scene (e.g., can’t find a spoon on a cluttered table).

5. Misreaching (optic ataxia).
   The hand reaches past or short of a visible object, making eating, pouring, or picking up items hard.

6. Ocular apraxia (trouble starting eye movements).
   The eyes hesitate or “stick,” making it hard to shift gaze or follow a line when reading.

7. Depth and distance errors.
   Stairs, curbs, and parking become hard. People step too high or too low or spill while pouring.

8. Getting lost (topographical disorientation).
   Navigation fails in new places and eventually in familiar neighborhoods or even inside the home.

9. Constructional apraxia (copying/drawing problems).
   Copying shapes, assembling furniture, or placing items symmetrically becomes very difficult.

10. Dyscalculia (number and layout problems).
    Balancing a checkbook, reading a clock, or aligning numbers in columns becomes confusing.

11. Left–right confusion and finger agnosia (Gerstmann features).
    People mix up left vs. right and cannot name fingers with eyes closed.

12. Crowding sensitivity and visual clutter intolerance.
    Supermarkets, busy screens, or patterned carpets overwhelm vision.

13. Visual illusions or misperceptions (occasionally hallucinations).
    In some (especially with Lewy pathology), people see shapes or people that are not there.

14. Anxiety and loss of confidence.
    The frightening mismatch—normal eye tests but real visual failure—drives anxiety and avoidance.

15. Later-stage memory and language difficulties.
    As disease spreads, more typical Alzheimer features (short-term memory loss, word-finding issues) appear.

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Diagnostic tests

The goal of testing is to: (1) prove the problem is in the brain’s visual networks, (2) exclude other treatable causes, and (3) identify the underlying disease (usually Alzheimer-type). Below are 20 commonly used tests with plain-English descriptions.

A) Physical examination

1. Neuro-ophthalmic examination.
   A clinician checks pupils, eye movements, tracking, and how the eyes work together. In VVAD, eye mechanics are often normal, but starting eye movements and scanning may be poor, revealing ocular apraxia.

2. Confrontation visual fields and neglect testing.
   The examiner brings fingers into view from different sides. People with posterior problems may miss items on one side or ignore one half of space (neglect), even when the eyes are fine.

3. Praxis examination (limb and dressing apraxia).
   Patients are asked to imitate gestures, use imaginary tools, or put on clothing. Errors point to parietal network problems involved in planning actions in space.

4. Gait and parkinsonism screen.
   Although not core, stiffness or slowness can hint at Lewy body or corticobasal pathology as the cause of a PCA-like syndrome.

B) Manual (bedside) cognitive tests

5. Montreal Cognitive Assessment (MoCA) with focus on visuospatial/executive tasks.
   Copying a cube, drawing a clock, and trail-making stress the posterior and fronto-parietal networks; these subtests are often impaired early.

6. Visual Object and Space Perception (VOSP) battery.
   Structured tasks measure object recognition and spatial perception, separating ventral (“what”) from dorsal (“where/how”) deficits.

7. Rey–Osterrieth Complex Figure (copy).
   Copying a complex figure tests global-to-local processing. Fragmented, piecemeal drawings suggest simultanagnosia.

8. Line bisection and star cancellation.
   People are asked to mark the middle of a line or cancel small targets across a page. Skewed or side-biased results show spatial attention problems.

9. Face and word tests (e.g., Benton Facial Recognition, reading lists).
   Difficulty matching unfamiliar faces or reading regular words points to ventral visual stream impairment.

C) Laboratory and pathological tests

10. Basic blood tests (TSH, B12, folate, CMP, CBC).
    These look for treatable contributors (thyroid problems, deficiencies, metabolic disorders) that can worsen thinking and vision.

11. Infection/autoimmune screen (as indicated).
    When the course is unusual or fast, doctors may test for syphilis, HIV, autoimmune encephalitis markers, or paraneoplastic antibodies to exclude mimics.

12. Cerebrospinal fluid (CSF) Alzheimer biomarkers.
    A lumbar puncture measures Aβ42 (low) and tau (elevated) patterns typical of Alzheimer’s disease, supporting VVAD due to AD.

13. Genetic testing (when early onset or strong family history).
    Rare PSEN1/APP/PSEN2 mutations are checked in appropriate families; results inform diagnosis and counseling.

D) Electrodiagnostic and physiologic tests

14. Electroencephalogram (EEG).
    Measures brain electrical activity. Helpful when the decline is rapid (to look for prion patterns) or when seizures are suspected.

15. Visual evoked potentials (VEP).
    Checks the signal from eye to brain. Often normal in VVAD (because the problem is beyond the earliest visual relay), which helps separate eye-pathway disease from cortical disease.

16. Polysomnography (sleep study) if Lewy features are suspected.
    Looks for REM sleep behavior disorder, which supports Lewy body pathology as the driver of a PCA-like presentation.

E) Imaging tests

17. MRI brain with volumetrics.
    Shows shrinkage (atrophy) in parietal/occipital regions and rules out strokes, tumors, or normal-pressure hydrocephalus. Advanced analysis can quantify posterior-dominant loss.

18. FDG-PET (glucose metabolism).
    Highlights reduced activity in the posterior cortex (parietal/occipital), a metabolic fingerprint of VVAD/PCA.

19. Amyloid PET.
    Detects amyloid-beta plaques. A positive scan supports Alzheimer-type pathology as the cause of the posterior syndrome.

20. Tau PET.
    Shows where tau tangles are concentrated. Posterior-heavy tau supports the VVAD/PCA pattern due to Alzheimer’s disease.

Non-pharmacological treatments (therapies & other approaches)

Below are practical, low-risk strategies that help people function better and stay safe. Evidence ranges from expert consensus, small studies, and real-world practice in PCA and low-vision rehabilitation.

1. Low-vision rehabilitation (OT/vision rehab):
   An occupational therapist trained in low vision teaches compensatory strategies: high-contrast labels, larger fonts, task lighting, decluttering, tactile markers on appliances, consistent item placement. Purpose: make everyday tasks doable and safer. Mechanism: reduces visual load and glare, boosts contrast, and replaces vision with touch/organization cues. PMC+2PMC+2

2. Home environment simplification:
   Clear walkways, remove loose rugs, use matte (not shiny) surfaces, color-contrast edges (e.g., dark placemat under a white plate), big-button remotes. Purpose: prevent falls and confusion. Mechanism: less visual clutter → easier object detection and navigation. Frontiers

3. Task lighting & glare control:
   Bright, even task lighting for reading and cooking; blinds/curtains or anti-glare films to cut reflections. Purpose: better visibility; less eye strain. Mechanism: improves signal-to-noise for visual processing. Spectrios Institute for Low Vision

4. High-contrast cues & signage:
   Use bold, simple signs (e.g., “BATHROOM →”), colored tape on stair edges, contrasting toilet seats, bold labels for cupboards. Purpose: quicker recognition and safer navigation. Mechanism: salient cueing of relevant targets. ResearchGate

5. Large-print and audio alternatives:
   Large-print books, e-reader zoom, text-to-speech, audiobooks, talking clocks/scales. Purpose: keep reading and timekeeping accessible. Mechanism: replaces or magnifies visual input. Alzheimer’s WA

6. Assistive technology:
   Smart speakers for voice commands, phone camera magnifier, GPS with voice navigation, smart-home routines. Purpose: independence and orientation. Mechanism: audio/tactile channels bypass strained visual processing. Rare Dementia Support

7. Cognitive rehabilitation (compensatory skills):
   Therapist-guided practice for dressing sequences, object search with fading cues, using checklists/routines. Purpose: maintain independence. Mechanism: procedural learning and habit formation despite visuospatial deficits. PMCUCL Discovery

8. Orientation routines:
   Set daily anchors (same breakfast spot, same route), visual calendars with high-contrast, and consistent storage places. Purpose: reduce anxiety and decision load. Mechanism: predictability reduces demand on visual scanning and working memory. PMC

9. Mobility training & fall prevention:
   Physiotherapy for balance, safe gait in busy or low-light areas, and use of handrails. Purpose: fewer falls and more confidence. Mechanism: motor strategies compensate for unreliable visual cues. PMC

10. Driving cessation & transport planning:
    Because spatial judgment and visual attention are impaired, driving becomes unsafe; clinicians advise stopping and planning alternatives (family help, rideshare, community transport). Purpose: safety for all. Mechanism: avoids high-risk tasks that depend on rapid visuospatial processing. (Driving fitness guidance emphasizes reporting and assessment.) Alzheimer’s SocietyGOV.UK

11. Caregiver education & support groups:
    Learning about PCA’s unique visual issues helps families adapt care and reduce frustration; rare-dementia support communities are valuable. Purpose: resilience, problem-solving. Mechanism: shared strategies and emotional support. University College London

12. Treat eye comorbidities (glasses, cataract care):
    Fixing reversible eye problems (refraction, cataract, dry eye) won’t cure PCA but improves usable vision. Purpose: maximize the visual input the brain receives. Mechanism: reduces optical blur competing with cortical issues. Alzheimer’s Research UK

13. Hearing assessment & aids if needed:
    Hearing loss worsens cognitive load and isolation. Treating hearing loss reduces dementia risk and improves communication now. Purpose: better cueing and social engagement. Mechanism: more reliable auditory channel when visual processing is weak. Spacecrafted

14. Exercise program (aerobic + strength + balance):
    Regular activity improves brain and vascular health, mood, sleep, and function. Purpose: slow decline and maintain mobility. Mechanism: neurotrophic, vascular, anti-inflammatory effects. CDC

15. Sleep optimization (sleep apnea screening, good sleep habits):
    Treat apnea; keep consistent sleep/wake times; morning light exposure. Purpose: clearer daytime thinking, steadier mood. Mechanism: restores circadian rhythms and oxygenation. The Lancet

16. Stress reduction & mental health care:
    Mindfulness, counseling, and treatment of depression/anxiety aid coping and participation in rehab. Purpose: better quality of life and function. Mechanism: reduces cognitive interference and improves motivation. Spacecrafted

17. Structured cognitive engagement:
    Simple, low-visual-load activities (music, conversation, podcasts, guided imagery, familiar crafts with tactile focus). Purpose: maintain cognitive reserve. Mechanism: stimulates non-visual networks. Spacecrafted

18. Nutrition pattern (Mediterranean/MIND-style):
    Food pattern rich in vegetables, berries, nuts, legumes, fish, whole grains, olive oil; low in ultra-processed foods. Purpose: support brain and heart health. Mechanism: anti-inflammatory, vascular, antioxidant effects. National Institute on AgingPMC

19. Air-quality and vascular risk control:
    Control blood pressure, diabetes, cholesterol, avoid smoke and pollution exposure when possible. Purpose: protect brain networks already under stress. Mechanism: reduces vascular and inflammatory hits. Spacecrafted

20. Personal safety planning:
    ID bracelet, fall alarms, medication organizers, and emergency plans. Purpose: prevent avoidable harm. Mechanism: adds non-visual safeguards to daily life. PMC

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Drug treatments

Important: medication plans must be individualized by a clinician who knows the person, comorbidities, MRI/PET results, and genetic risk (especially APOE ε4)—this matters for safety monitoring of disease-modifying antibodies.

1. Donepezil (cholinesterase inhibitor)

• Dose/time: start 5 mg nightly; typical 10 mg nightly.

• Purpose: support attention/executive function and day-to-day activities; some people with PCA report better task performance.

• Mechanism: boosts acetylcholine signaling.

• Side effects: nausea, vivid dreams, bradycardia; rare heart block. (Applies broadly to AD; used off-label in PCA.) PMC

2. Rivastigmine (cholinesterase inhibitor) (capsules or patch)

• Dose/time: oral titrated to 6–12 mg/day divided; patch 4.6 → 9.5 → 13.3 mg/24 h once daily.

• Purpose/mechanism/side effects: as above; patch may cause fewer GI effects but can irritate skin. PMC

3. Galantamine (cholinesterase inhibitor)

• Dose/time: 16–24 mg/day (ER once daily or divided).

• Purpose: similar goals as above.

• Side effects: GI upset, weight loss; caution with cardiac conduction issues. PMC

4. Memantine (NMDA receptor antagonist)

• Dose/time: 10 mg twice daily (or XR 28 mg daily).

• Purpose: for moderate stages or added to cholinesterase inhibitor; may reduce agitation/irritability.

• Mechanism: reduces glutamate-related excitotoxicity.

• Side effects: dizziness, headache, constipation. PMC

5. Lecanemab (Leqembi®; anti-amyloid monoclonal antibody)

• Dose/time: 10 mg/kg IV every 2 weeks (initiation). After ~18 months, FDA-approved maintenance options: 10 mg/kg IV every 4 weeks or 360 mg subcutaneous weekly (IQLIK autoinjector), if appropriate.

• Purpose: disease-modifying therapy that slows decline in early AD (MCI or mild dementia) with confirmed amyloid; applicable if VVAD is Alzheimer’s-mediated and meets criteria.

• Mechanism: binds amyloid beta → facilitates plaque clearance.

• Safety: ARIA (brain swelling/bleeds) risk—higher in APOE ε4 carriers; MRI monitoring required per label. FDA Access DataLeqembiPractical Neurology

6. Donanemab (Kisunla™; anti-amyloid monoclonal antibody)

• Dose/time (current label): 700 mg IV every 4 weeks for 3 doses, then 1400 mg every 4 weeks; titration regimens have been studied and a label update with a titration schedule was approved in 2025.

• Purpose: disease-modifying in early AD with confirmed amyloid; relevant in VVAD due to AD.

• Mechanism: targets a pyroglutamate Aβ form; promotes amyloid removal.

• Safety: ARIA risk; MRI monitoring per FDA label. U.S. Food and Drug AdministrationLilly Investor Relations+1FDA Access Data

7. SSRIs (e.g., sertraline, citalopram) for depression/anxiety

• Dose/time: typical SSRI dosing (e.g., sertraline 25–100 mg/day).

• Purpose: treat mood/anxiety that worsen function and caregiver stress; improves participation in rehab.

• Mechanism: increases serotonin signaling.

• Side effects: GI upset, sleep change, hyponatremia in older adults. (Use in dementia is common; dosing individualized.) Spacecrafted

8. Melatonin for sleep/circadian rhythm

• Dose/time: 1–3 mg at bedtime (titrate by clinician).

• Purpose: improve sleep quality; better daytime alertness.

• Mechanism: supports circadian signaling.

• Side effects: morning grogginess (usually mild). Spacecrafted

9. Short-term anxiolytics (careful use)

• Dose/time: clinician-guided; avoid long-term benzodiazepines.

• Purpose: acute anxiety/panic that blocks rehab.

• Mechanism/side effects: sedation, falls, confusion—use sparingly and prefer non-drug options first. PMC

10. Treatment of vascular risks (statins, antihypertensives, diabetes meds)

• Purpose: brain protection when vascular risks coexist.

• Mechanism: improves cerebrovascular health, which supports cognition.

• Note: regimen must be individualized for comorbidities. Spacecrafted

Aducanumab (Aduhelm®) was discontinued by the manufacturer in 2024; patients were transitioned off by late 2024. Alzheimer’s AssociationAmerican Academy of NeurologyNCBI

Coverage & logistics: In the U.S., Medicare expanded coverage for lecanemab after full FDA approval, with registry/monitoring requirements; donanemab was FDA-approved on July 2, 2024. These are specialty therapies that require memory-clinic oversight. Centers for Medicare & Medicaid ServicesU.S. Food and Drug Administration

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Dietary molecular supplements

Evidence for supplements is mixed. Discuss with your clinician—especially to check interactions and kidney/liver health. Use supplements to support (not replace) medical care and a healthy diet.

1. Omega-3 DHA/EPA (fish oil): 1–2 g/day combined EPA+DHA.
   Function: anti-inflammatory; supports neuronal membranes. Mechanism: membrane fluidity and anti-inflammatory lipid mediators. Evidence modest but supportive for brain and vascular health.

2. Vitamin D3: 800–2000 IU/day (dose per blood level).
   Function: bone, immune, and possibly cognitive support. Mechanism: neurosteroid and immune modulation.

3. Vitamin B12 (± folate, B6 if deficient): dose per deficiency (e.g., B12 1000 µg/day orally or injections).
   Function: corrects deficiency that can worsen cognition. Mechanism: homocysteine reduction and myelin support.

4. Magnesium glycinate/citrate: 200–400 mg elemental/day (adjust for kidneys).
   Function: sleep, muscle relaxation. Mechanism: NMDA modulation.

5. Curcumin (with piperine or formulated for absorption): 500–1000 mg/day.
   Function: antioxidant/anti-inflammatory; human AD evidence limited; consider as adjunct. Mechanism: NF-κB and amyloid aggregation modulation (preclinical).

6. CoQ10 (ubiquinone or ubiquinol): 100–200 mg/day.
   Function: mitochondrial support, antioxidant. Mechanism: electron transport.

7. Resveratrol: 100–200 mg/day.
   Function: antioxidant; limited human cognitive data. Mechanism: SIRT1 activation (preclinical).

8. Phosphatidylserine: 100 mg 2–3×/day.
   Function: membrane phospholipid; small trials suggest attention benefits in some older adults. Mechanism: membrane signaling.

9. Lutein/zeaxanthin: per label (e.g., lutein 10 mg + zeaxanthin 2 mg/day).
   Function: macular pigments; supports visual processing by improving retinal signal quality. Mechanism: antioxidant in retina.

10. Probiotic fiber (inulin/psyllium) & fermented foods: as tolerated.
    Function: gut-brain axis, metabolic health. Mechanism: short-chain fatty acids and reduced inflammation.

(For all: consistent diet patterns like Mediterranean/MIND have stronger evidence than single supplements.) National Institute on AgingPMC

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Regenerative / stem-cell-related” therapies

Plain truth: there are no approved stem-cell drugs for Alzheimer’s, including VVAD, at this time. What is available are passive immunotherapies (monoclonal antibodies against amyloid) that slow decline in early Alzheimer’s. The items below explain the landscape and the current evidence/status.

1. Lecanemab (passive immunotherapy, anti-amyloid; approved):
   Dose/Mechanism/Safety as above. “Immunity-based” because it uses antibodies to clear amyloid. Requires MRI monitoring for ARIA. FDA Access Data

2. Donanemab (passive immunotherapy; approved):
   Dose/Mechanism/Safety as above; label includes titration information; MRI monitoring required. FDA Access Data

3. Anti-tau monoclonal antibodies (e.g., semorinemab, tilavonemab; research):
   Purpose: target tau proteins that form tangles. Status: mixed/negative primary outcomes so far; ongoing trials refine targets and timing.

4. Active amyloid/tau vaccines (e.g., CAD106, UB-311; research):
   Purpose: teach the immune system to make antibodies. Status: early-to-mid trials; not approved.

5. Microglial/innate immune pathway drugs (e.g., TREM2 modulators; research):
   Purpose: adjust brain immune cells to clear pathology with less inflammation. Status: early trials.

6. Cell-based therapies (mesenchymal or neural stem cells; research/experimental only):
   Purpose: trophic support or replacement. Status: not approved for AD; if you see offers for stem-cell “cures,” be cautious and discuss with a neurologist.

Summary: The only disease-modifying immunotherapies available in routine practice right now are lecanemab and donanemab, approved for early Alzheimer’s with confirmed amyloid. They require strict safety monitoring and specialist oversight. U.S. Food and Drug AdministrationCenters for Medicare & Medicaid Services

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Surgeries

There is no brain surgery proven to treat VVAD/PCA. However, certain procedures may be considered for other conditions that can worsen visual function or resemble PCA:

1. Cataract surgery (if cataract present): improves retinal image quality, helping remaining visual processing. Not a treatment for PCA itself. (Why: remove clouded lens to maximize usable vision.) Alzheimer’s Research UK

2. Glaucoma procedures (if glaucoma present): lowers eye pressure to protect optic nerve. (Why: prevent additional vision loss unrelated to PCA.)

3. Retinal procedures (if separate retinal disease present): e.g., injections/laser for macular disease. (Why: preserve the eye’s signal to help the brain use whatever vision remains.)

4. Sleep-apnea therapy equipment (non-surgical but procedural): e.g., CPAP setup; some cases may consider ENT procedures for airway if indicated. (Why: better sleep and cognition.) Spacecrafted

5. Shunt surgery (only if misdiagnosed normal-pressure hydrocephalus is actually present): not for PCA, but included here so teams rule it in/out. (Why: treatable cause of gait/cognition/urinary issues distinct from PCA.)

Bottom line: surgery does not treat VVAD. Procedures are about coexisting conditions.

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Prevention & risk-reduction actions

These steps reduce overall dementia risk and protect brain networks under stress. They cannot guarantee prevention but do help population-level risk.

1. Control blood pressure (aim per doctor’s guidance).

2. Manage diabetes and keep A1c in target.

3. Treat hearing loss (hearing aids if needed).

4. Correct vision problems (glasses, cataract care).

5. Be physically active (≥150 minutes/week moderate activity).

6. Mediterranean/MIND-style diet; limit ultra-processed food.

7. Don’t smoke; avoid secondhand smoke and pollution exposure.

8. Limit alcohol (or avoid).

9. Protect your head (seatbelts, helmets; avoid repetitive head injury).

10. Stay socially and mentally active (engage daily). The LancetSpacecraftedCDCUniversity College London

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When to see doctors (red flags & timing)

• Right away if there’s sudden confusion, new weakness, new severe headache, loss of vision in one eye, or a sudden big drop in function (possible stroke or other acute issue).

• Promptly if visual confusion becomes dangerous (near falls, kitchen accidents), if there are new hallucinations, severe sleep problems, or major mood/behavior changes.

• Soon for a structured memory-clinic evaluation if you or family notice persistent visuospatial problems (getting lost, misreaching, difficulty reading or dressing) for >3–6 months, especially if routine eye exams are normal.

• Before starting any disease-modifying therapy (lecanemab/donanemab), to confirm amyloid positivity, stage (MCI/mild dementia), MRI safety, and to set up MRI monitoring for ARIA. FDA Access Data

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What to eat and what to avoid

What to eat more of :

1. Leafy greens & colorful vegetables daily (spinach, kale, peppers).

2. Berries (blueberries, strawberries) several times per week.

3. Nuts & seeds (walnuts, almonds, flax/chia) for healthy fats.

4. Fish (especially oily fish like sardines or salmon) 1–2×/week.

5. Whole grains & legumes (oats, brown rice, lentils) as staples. National Institute on AgingBioMed Central

What to limit/avoid :

1. Ultra-processed foods (chips, packaged sweets, fast food).

2. Sugary drinks and excess refined starches.

3. High-saturated-fat meats and processed meats.

4. Excess salt if you have hypertension.

5. Heavy alcohol; if you drink, keep it light and physician-approved. ScienceDirect

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FAQs

1) Is VVAD the same as typical Alzheimer’s?
It’s caused by similar Alzheimer’s changes, but symptoms start in the visual brain areas first, so seeing/processing the world is the main early problem. Memory loss can come later. NCBI

2) Can eye surgery or new glasses cure it?
No. The eyes may be healthy; the problem is in the brain’s visual system. But correcting eye issues (glasses, cataract) can maximize the vision you do have. Alzheimer’s Research UK

3) What brain scans are useful?
MRI often shows shrinkage at the back of the brain; FDG-PET shows low metabolism there; amyloid PET/tau PET or spinal fluid can confirm Alzheimer’s pathology. PMC

4) Can medications help?
Yes. Standard Alzheimer’s meds (donepezil/rivastigmine/galantamine ± memantine) can help some symptoms. Lecanemab and donanemab can slow decline in early, amyloid-positive disease but require MRI monitoring for side effects. FDA Access DataU.S. Food and Drug Administration

5) What is ARIA and why do I need MRIs?
ARIA is brain swelling or small bleeds seen in some people receiving anti-amyloid antibodies. It is often mild but can be serious; MRI checks are part of safe treatment. FDA Access Data

6) Are stem cells a cure?
No approved stem-cell therapies exist for Alzheimer’s/PCA. Stem-cell approaches are experimental only. National Institute on Aging

7) Will I have to stop driving?
Often, yes. The condition affects spatial judgment, visual attention, and reaction time, so driving becomes unsafe. Plan alternatives early. Alzheimer’s Society

8) Do vision aids really help?
Yes—high contrast, bigger print, better lighting, labels, simplified spaces, audio aides—all can reduce daily errors and stress. PMC

9) Can diet make a difference?
Patterns like Mediterranean/MIND are linked with slower decline and lower risk; they support overall brain and heart health. National Institute on AgingPMC

10) Should I treat hearing loss?
Definitely. Hearing support improves communication and may reduce dementia risk. Spacecrafted

11) Is VVAD rare?
Yes, it’s less common than typical memory-led Alzheimer’s, which is why specialized centers may help. The Lancet

12) Why do I bump into things even with good eye tests?
Because the brain has trouble locating and interpreting objects and distances—this is a processing problem, not just “blurry vision.” NCBI

13) Will memory stay normal?
Memory is usually relatively better early, but declines over time as disease spreads. The Lancet

14) How do we plan care?
Use occupational therapy, home safety changes, caregiver training, transport planning, and consider disease-modifying therapy if eligible. PMC

15) What’s the outlook?
It’s a progressive condition. The goal is to slow decline, reduce hazards, and preserve independence and dignity with the best mix of therapies, supports, and (when appropriate) immunotherapy. The Lancet

Disclaimer: Each person’s journey is unique, treatment plan, life style, food habit, hormonal condition, immune system, chronic disease condition, geological location, weather and previous medical  history is also unique. So always seek the best advice from a qualified medical professional or health care provider before trying any treatments to ensure to find out the best plan for you. This guide is for general information and educational purposes only. Regular check-ups and awareness can help to manage and prevent complications associated with these diseases conditions. If you or someone are suffering from this disease condition bookmark this website or share with someone who might find it useful! Boost your knowledge and stay ahead in your health journey. We always try to ensure that the content is regularly updated to reflect the latest medical research and treatment options. Thank you for giving your valuable time to read the article.

The article is written by Team RxHarun and reviewed by the Rx Editorial Board Members

Last Updated: August 30, 2025.