Aetna Alzheimer's Disease Tests Coverage Update

Medically Necessary

Medically necessary tests — Covered when ALL of the following are met:

ALL of the following

Lumbar puncture for cerebrospinal fluid (CSF) analysis demonstrating elevated phosphorylated tau (P-tau) and/or elevated total tau (T-tau) and reduced Aβ42 or low Aβ42/Aβ40 ratio as determined by the laboratory assay for assessment of mild cognitive impairment (MCI) when Alzheimer's disease (AD) is suspected.
Brain magnetic resonance imaging (MRI) performed for indications related to initiation or monitoring of Aduhelm or Leqembi per referenced CPBs (e.g., within one year prior to therapy initiation, or to evaluate for amyloid-related imaging abnormalities at specified dosing intervals).
Genetic mutation testing for APP, PSEN1, or PSEN2 in members with MCI or mild AD dementia who are <50 years of age and being considered for enrollment in clinical trials of aducanumab or lecanemab, when trial eligibility requires such testing.

Experimental and Investigational

Experimental and investigational — The following tests/measurements are considered experimental and investigational for the diagnosis and/or assessment of Alzheimer's disease and related dementias because their clinical value remains unproven for these indications:

ALL of the following

Apolipoprotein E (apoE) genotyping.
ATP-binding cassette transporter (ABCA7) testing.
Automated computerized cognitive assessment aids as standalone diagnostic tools.
Bcl-2 rs956572 polymorphism testing.
Plasma beta-amyloid 42 (Aβ42).
Beta-site amyloid precursor protein cleaving enzyme 1 (BACE1) and CSF β-secretase activity.

CSF β-Secretase Activity (not useful in preclinical staging)

CSF β-secretase activity (diagnostic support) — Summary of evidence-based coverage-relevant findings:

ALL of the following

Cross-sectional multicenter data (SIGNAL cohort) including 266 cognitively normal volunteers found no differences in CSF sAPPβ or β-secretase activity across pre-clinical AD stages (0,1,2-3) and SNAP, suggesting these markers do not distinguish early preclinical stages.
Age correlated with established markers (t-tau, p-tau, YKL-40) and with Aβ42 in APOE ε4 carriers, but not with sAPPβ or β-secretase activity, limiting their utility as stage indicators.
Authors concluded sAPPβ and β-secretase activity are not useful diagnostic or staging markers in pre-clinical AD.
Clinical guidance summaries (UpToDate) note that molecular biomarkers are supportive but currently limited to investigational use and are not valid as stand-alone diagnostic tests; testing is not universally available or reimbursed.

Circadian Rhythm Analysis (emerging biomarker)

Circadian rhythm analysis (emerging biomarker) — Summary of evidence-based coverage-relevant findings:

ALL of the following

Actigraphy studies in cognitively normal adults (n≈189 analyzed) showed that pre-clinical amyloid pathology (positive PiB or higher CSF p-tau/Aβ42 ratio) was associated with increased intra-daily variability (rest-activity fragmentation) independent of age and sex.
Older age and male sex were independently associated with circadian dysfunction measures; findings could be confounded by unmeasured sleep disorders (e.g., sleep apnea), medications, comorbidities, and non-circadian behaviors such as exercise.
Authors concluded circadian rhythm abnormalities may contribute to early AD pathogenesis or serve as a potential biomarker of pre-clinical disease, but replication and confirmation with additional circadian parameters and longitudinal data are needed.

Summarized Evidence-Based Findings

Summarized evidence-based findings — Group-level diagnostic performance and limitations reported in the document:

ALL of the following

CSF synaptic biomarkers (neurogranin, SNAP-25 variants, GAP-43, synaptotagmin-1) show elevated levels in AD and have demonstrated discriminatory ability (AUCs often ≥0.80) between AD and non-AD disorders in multiple cohorts, with some markers (e.g., SNAP-25aa40, p-tau T217) showing high accuracy in select studies.
CSF p-tau assays (including novel targets such as p-tau T217) have shown improved diagnostic accuracy compared with earlier p-tau assays, with reported sensitivities and specificities in many studies exceeding 85–90% for distinguishing AD from controls or other dementias in research settings.
Blood biomarkers (plasma p-tau species, plasma GFAP, plasma p-tau231/p-tau181, plasma total tau) show promise for identifying AD pathology at group level, but substantial overlap with normal aging and other conditions limits individual-level diagnostic certainty; plasma GFAP may rise early in preclinical AD cohorts.
Serum NfL is a sensitive marker of neurodegeneration and correlates with disease stage and progression in familial AD cohorts, but it is not specific to AD and increases in multiple neurologic conditions, limiting its use as a standalone diagnostic test.

Evidence Summaries / Implied Coverage Stance

Evidence summaries / implied coverage stance — Key limitations and policy implications derived from the evidence:

ALL of the following

Most novel CSF and blood biomarkers demonstrate promising group-level associations with AD pathology but lack prospective, multi-center, longitudinal studies showing that testing changes clinical management and improves outcomes; therefore, routine clinical use is not supported for many of these assays.
None of the investigational tests identified are valid as stand-alone diagnostic tests for AD; use is primarily limited to research settings and clinical trials until standardized assays, validated thresholds, and demonstrated impact on management are available.
Where markers have shown higher diagnostic accuracy (e.g., CSF p-tau T217, certain CSF synaptic markers), their integration into clinical practice should await consensus on assay standardization, external validation, and demonstration of clinical utility and cost-effectiveness.
Some biomarkers (e.g., CSF Aβ42/Aβ40 ratio, CSF total and phosphorylated tau, amyloid PET) are incorporated in research diagnostic frameworks and may be used in specific clinical circumstances (eg, early-onset dementia, atypical presentations, or when results would affect management), consistent with the medically necessary criteria stated elsewhere in this policy.

Coding and Billing Guidance

Covered CPT/HCPCS (if selection criteria met) and related codesmixedCovered

0358U	Neurology (mild cognitive impairment), analysis of B-amyloid 1-42 and 1-40, chemiluminescence enzyme immunoassay, cerebral spinal fluid, reported as positive, likely positive, or negative.
62270	Spinal puncture, lumbar, diagnostic
70551	Magnetic resonance (eg, proton) imaging, brain (including brain stem); without contrast material.
70552	Magnetic resonance (eg, proton) imaging, brain (including brain stem); with contrast material(s).
70553	Magnetic resonance (eg, proton) imaging, brain (including brain stem); without contrast material, followed by contrast material(s) and further sequences.
81405	Molecular pathology procedure, Level 6 full gene sequence PSEN1 (presenilin 1) (eg, Alzheimer disease).
81406	Molecular pathology procedure, Level 7 full gene sequence APP (amyloid beta [A4] precursor protein) (eg, Alzheimer disease), full gene sequence PSEN2 (presenilin 2 [Alzheimer disease 4]) (eg, Alzheimer disease).
83520	Immunoassay for analyte other than infectious agent antibody or infectious agent antigen; quantitative, not otherwise specified.
78608	Brain imaging, positron emission tomography (PET); metabolic evaluation.
88271	Molecular cytogenetics.

1–10 of 17

1/2

CPT/HCPCS codes listed as not covered for CPB indications or relatedmixedNot Covered

0206U	Neurology (Alzheimer disease); cell aggregation using morphometric imaging and protein kinase C-epsilon (PKCe) concentration in response to amylospheroid treatment by ELISA, cultured skin fibroblasts, each reported as positive or negative for Alzheimer disease.
+0207U	Disease quantitative imaging of phosphorylated ERK1 and ERK2 in response to bradykinin treatment by in situ immunofluorescence, using cultured skin fibroblasts, reported as a probability index for Alzheimer disease (List separately in addition to code for primary procedure).
0289U	Neurology (Alzheimer disease), mRNA, gene expression profiling by RNA sequencing of 24 genes, whole blood, algorithm reported as predictive risk score.
81401	Molecular pathology procedure, Level 2 (eg, 2-10 SNPs, 1 methylated variant, or 1 somatic variant [typically using nonsequencing target variant analysis], or detection of a dynamic mutation disorder/triplet repeat).
82172	Apolipoprotein, each.
82465	Cholesterol, serum or whole blood, total.
82530	Cortisol; free [long-term measurement of cortisol].
82533	Cortisol; total [long-term measurement of cortisol].
82728	Ferritin.
83090	Homocysteine.

1–10 of 17

1/2

HCPCS covered if selection criteria are metHCPCSCovered

S3852

DNA analysis for APOE epsilon 4 allele for susceptibility to Alzheimer’s disease.

ICD-10 codes covered if selection criteria are metICD-10Covered

F01.50 - F03.C4	Dementia [For age less than 50 years].
G30.0 - G30.9	Alzheimer’s disease.
G31.84	Mild cognitive impairment, so stated.
I68.0	Cerebral amyloid angiopathy.
R90.89	Other abnormal findings on diagnostic imaging of central nervous system.
R94.02	Abnormal brain scan.

ICD-10 codes not covered for listed indicationsICD-10Not Covered

Z13.858	Encounter for screening for other nervous system disorders [screening for dementia].
Z82.0	Family history of epilepsy and other diseases of the nervous system [family history of Alzheimer’s disease].

MRI timing for ARIA monitoring — therapy-specific

Aducanumab (Aduhelm) — ARIA-monitoring MRI timingMRI prior to the 5th, 7th, 9th, and 12th aducanumab dose

Lecanemab (Leqembi) — ARIA-monitoring MRI timingMRI prior to the 5th, 7th, and 14th lecanemab dose

PurposeEvaluate for evidence of amyloid-related imaging abnormalities (ARIA) during therapy

MRI pre-initiation

RequirementBrain MRI within one year prior to initiating Aduhelm or Leqembi

ContextUsed to indicate AD prior to starting aducanumab-avwa or lecanemab-irmb therapy

Related guidanceSee CPB 0996 (Aduhelm) and CPB 1026 (Leqembi) for full therapy monitoring protocols

Genetic testing age threshold

Age thresholdMembers less than 50 years of age

Clinical stateMCI or mild AD dementia

Indication for testingBeing considered for enrollment in a clinical trial of Aduhelm or Leqembi

CSF VILIP-1

VILIP-1 threshold>= 560 pg/ml (upper tercile)

Prognostic significanceUpper tercile (>=560 pg/ml) associated with more rapid clinical decline in CDR-SB and global scores

Study contextFindings from longitudinal cohort of very mild/mild AD with mean follow-up ~2.6 years

Provider Responsibilities, Prior Authorization, and Documentation

Prior Authorization

Imaging and CSF testing prior auth considerations — Therapy monitoring imaging steps

Brain MRI and CSF testing used in association with initiation and monitoring of aducanumab (Aduhelm) or lecanemab (Leqembi) have specific timing and documentation expectations. A brain MRI is required within one year prior to initiating Aduhelm or Leqembi to indicate AD, and additionally prior to specific dose milestones to evaluate for amyloid-related imaging abnormalities (ARIA): prior to the 5th, 7th, 9th, and 12th aducanumab dose and prior to the 5th, 7th, and 14th lecanemab dose. Lumbar puncture for CSF biomarkers (Aβ42, Aβ40 ratio, total tau, phosphorylated tau) may be medically necessary for assessment of MCI when AD is suspected but results and interpretation must be documented in the medical record. Providers should obtain and retain imaging and CSF reports in the member's chart to support medical necessity when submitting claims.

MRI timing: within 12 months pre-initiation; before 5th, 7th, 9th, 12th Aduhelm doses; before 5th, 7th, 14th Leqembi doses
CSF LP: indicated to confirm elevated p-tau and/or t-tau and reduced Aβ42 or low Aβ42/Aβ40 ratio for MCI when AD is suspected

Note

Prior authorization — regulatory note

This Clinical Policy Bulletin is intended to assist in administering plan benefits and does not itself establish prior authorization requirements. Specific prior authorization and benefit determinations are governed by the member's plan documents and any program disclosures; providers must follow plan provisions and submit prior authorization requests where required by the member's contract.

Clinical Policy Bulletins do not constitute offers of coverage
Prior authorization requirements are determined by the member’s benefit plan

Denial Risk

Investigational / reimbursement caution

Many emerging biomarker tests (blood-based assays, proprietary panels, skin biopsy assays, novel CSF analytes) remain investigational or of limited clinical validation and are not universally reimbursed. Use of such tests may require prior authorization in some plans and may be denied if clinical utility or FDA-cleared/approved status is lacking.

Examples: MindX blood mRNA panel, NeuroDiagnostics Discern skin biopsy, Syn-One cutaneous alpha‑synuclein testing
Testing availability and reimbursement vary; check payer-specific prior authorization rules

Prior Authorization

Investigational tests may need prior authorization

Investigational tests (proprietary or not yet validated assays) may trigger prior authorization reviews or medical necessity denials. When ordering such tests, providers should verify plan coverage and submit documentation demonstrating why testing is required for patient management if prior authorization is requested.

Prior authorization may be requested for investigational blood or skin-based AD biomarker tests
Submit clinical rationale and supporting records when prior auth is required

Note

Not applicable in this document segment

No step therapy requirements are described in this document segment.

Denial Risk

Regulatory status implication

There are currently no FDA-approved in‑vitro diagnostics (IVDs) universally accepted for early detection of AD; absence of FDA-cleared tests or guideline endorsement increases the risk of noncoverage for experimental assays.

No FDA-approved IVDs for early detection of AD noted in this bulletin
Lack of regulatory approval may lead to denial or no reimbursement

Denial Risk

Investigational status and reimbursement risk

Testing for many novel biomarkers remains investigational and is not universally reimbursed by most insurers. Providers should be aware that clinical utility is not established for numerous blood analytes, skin biopsy biomarkers, and some CSF analytes; reimbursement may be denied absent convincing evidence and plan coverage.

Examples of investigational/limited-evidence tests listed in the policy: plasma Aβ42, CSF VILIP‑1, various CSF synaptic biomarkers, blood neurodegenerative analytes, Syn‑One cutaneous alpha‑synuclein
Testing may be limited to research settings or clinical trials

Denial Risk

Established use limitations

Certain tests have limited or unestablished roles (for diagnosis, monitoring, or therapy response). For example, the NeuroDiagnostics skin biopsy AD biomarker assays have not been established for monitoring responses to therapies; Syn‑One cutaneous alpha‑synuclein testing lacks guideline endorsement for AD management.

NeuroDiagnostics Discern: safety and effectiveness not established for monitoring therapy response
Syn‑One and similar peripheral tests: not described in key UpToDate reviews; absence from guidelines may trigger coverage denial

Note

Not applicable in this excerpt — no explicit prior authorization rules present

No explicit prior authorization rules are present in this excerpt for many individual tests; however, absence of payer-specific prior authorization language in the bulletin does not imply coverage. Providers must consult the member’s benefit plan and prior authorization resources.

Denial Risk

Guideline/gold-standard absence may trigger denial

When tests lack guideline or gold-standard support (for example, Syn‑One cutaneous alpha‑synuclein testing or proprietary risk-score algorithms without independent validation), payers may deny coverage. Providers should document why such testing is clinically necessary and reference supporting evidence when available.

Absence from AAN/UpToDate guidance or major clinical guidelines increases denial risk
Provide literature or trial justification if requesting coverage for nonstandard tests

Documentation Required

Clinical indication documentation

Document the clinical indication for testing: suspected AD or MCI, atypical presentation, early-onset (<50 years) considerations for genetic testing related to trial enrollment, or need for confirmation before initiating disease-modifying therapies (e.g., Aduhelm or Leqembi). For therapy-related imaging or CSF testing, document timing relative to initiation and dosing milestones.

Indications to document: suspected AD, MCI with suspected AD, atypical presentation, early-onset dementia (<50 years) when considering genetic testing for APP/PSEN1/PSEN2 for trial enrollment
Document relation to therapy initiation and monitoring (Aduhelm/Leqembi dosing schedule)

Documentation Required

Clinical measurement notes

When reporting biomarker results, include measurement methods and thresholds where applicable (e.g., CSF VILIP‑1 ≥560 pg/mL associated with more rapid decline in one study) and note that biomarker ratios such as p‑tau/Aβ42 or t‑tau/Aβ42 often provide better diagnostic discrimination than single analytes.

Report specific analyte values and any lab-specific cutoffs or ratios (p‑tau/Aβ42, t‑tau/Aβ42, Aβ42/Aβ40)
Example: CSF VILIP‑1 ≥560 pg/mL associated with faster cognitive decline in early AD cohort

Documentation Required

Reporting confounders for CSF biomarker interpretation

Reports interpreting CSF biomarker results should include potential confounders that affect diagnostic performance: patient age, disease duration, and degree of cognitive impairment. Studies recommend reporting these variables to aid interpretation.

Key confounders: age, disease duration, global cognitive impairment (e.g., MMSE), and timing relative to symptom onset
Note whether CSF and/or amyloid PET confirmation was available

Documentation Required

Required clinical documentation for CSF biomarker use

Required clinical documentation when using CSF biomarkers: indication for testing, description of symptoms and cognitive testing results, imaging findings if available, laboratory method/assay used (including whether automated validated platforms were used), and how results will affect patient management. CSF biomarkers should support but not replace clinical assessment.

Include symptom description, cognitive testing scores, and imaging findings
Document assay platform (e.g., automated Elecsys) and lab performing the test
State how results will change management (diagnosis confirmation, trial eligibility, therapy decision)

Billing Rule

Specimen and report requirements

Vendor-proprietary tests require a prescription and submission of specific specimen types and processing instructions. For example, the MindX blood mRNA panel and NeuroDiagnostics Discern skin biopsy are prescription-only and have vendor-specific specimen requirements and turnaround processes; providers must follow manufacturer/laboratory instructions and include required clinical information on the order.

MindX: whole blood RNA sequencing of 24 genes — prescription required
NeuroDiagnostics Discern: 2–3 mm skin punch biopsy from bicep/forearm — specimen handling and culture grown per vendor instructions

Documentation Required

Recommended documentation elements (research/clinical studies)

When ordering and documenting investigational or research-oriented biomarker testing, include the elements commonly reported in published studies: raw analyte concentrations, ratios (p‑tau/Aβ42, t‑tau/Aβ42, Aβ42/Aβ40), assay platform and validation status (e.g., Simoa, automated immunoassay), and comparison group details if relevant. Indicate whether results were corroborated by CSF or amyloid PET when available.

Document analytes measured (GFAP, p‑tau181, p‑tau231, NfL, Aβ42, Aβ40, total tau) and assay used (eg, Simoa, Elecsys)
Include group characteristics and reference ranges where reported

Documentation Required

Document study limitations and lack of biomarker confirmation

Study reports frequently note limitations that affect clinical generalizability: cross-sectional design, small sample sizes, lack of amyloid PET or CSF confirmation in all participants, and limited ethnic diversity. Providers should acknowledge such limitations in justification for testing and when interpreting results.

Common limitations: cross-sectional data, lack of confirmatory PET/CSF, small or homogeneous cohorts, differences in assay methods between studies
Include these limitations when submitting rationale for testing

Documentation Required

Provider responsibilities

Treating providers are responsible for following plan provisions, obtaining required authorizations, documenting medical necessity, and managing member care. Clinical Policy Bulletins are an administrative tool and do not replace provider judgment. Providers should ensure records support services billed and be prepared to supply documentation for prior authorization or appeals.

Providers remain solely responsible for medical advice and treatment
Follow plan prior authorization procedures and retain documentation to support claims

Note

Genetic testing guidance

Genetic testing guidance: routine APOE genotyping and broad genetic testing are not recommended for routine evaluation of dementia. Genetic mutation testing for APP, PSEN1, or PSEN2 may be appropriate for individuals with MCI or mild AD dementia who are younger (for example, <50 years) and are being considered for enrollment in clinical trials of aducanumab or lecanemab; document age, clinical context, and trial consideration when ordering.

AAN and UpToDate do not recommend routine APOE genotyping for AD diagnosis
Consider APP/PSEN1/PSEN2 testing in early-onset cases being evaluated for clinical trial eligibility

Definitions and Key Terms

Mild cognitive impairment (MCI)

DefinitionMild cognitive impairment (MCI) is a transitional state between normal aging and dementia

Risk of progressionIndividuals with MCI have an increased annual risk (~12% per year) of progressing to AD

Clinical useMCI evaluation may include CSF biomarkers when AD is suspected

CSF biomarkers

ComponentsCSF measures include phosphorylated tau (p-tau), total tau (t-tau), and beta-amyloid 42 (Aβ42) or Aβ42:Aβ40 ratio

Diagnostic roleThese biomarkers can be supportive of an AD diagnosis but are not recommended for routine standalone use

Clinical contextsUseful in early-onset or atypical presentations and for differential diagnosis vs FTLD

Early-onset familial Alzheimer disease (EOFAD)

DefinitionEarly-onset familial Alzheimer disease (EOFAD) — rare AD with onset between ages ~30 and 60

Genetic causesMost often caused by mutations in APP, PSEN1, or PSEN2

Testing contextGenetic testing considered for suspected EOFAD or trial enrollment under age-based criteria

CSF biomarkers (diagnostic use)

ComponentsCSF Aβ42, total tau (t-tau), and phosphorylated tau (p-tau) used to assess AD pathology

InterpretationRatios (eg, p-tau/Aβ42) may improve diagnostic performance and should account for confounders like age and disease duration

LimitationsBiomarkers are supportive but not definitive; standardization and reporting of assay methods recommended

TREM2 R47H (rs75932628)

VariantTREM2 R47H (rs75932628)

Association with ADRare missense variant associated with increased risk of late-onset Alzheimer disease (combined OR ≈ 2.9)

EvidenceIdentified in genome/exome sequencing studies with replication across cohorts

p-tau T217

Analytep-tau T217 (CSF)

PerformanceNovel Simoa immunoassay showed higher diagnostic accuracy for AD compared with p-tau T181 in cohort studies

Assay cut-off exampleReported cut-off 242 pg/ml with ~90% accuracy in a 190-subject cohort

CSF synaptic biomarkers

MarkersCSF synaptic biomarkers include neurogranin (NGRN), SNAP-25, GAP-43, synaptotagmin-1

Diagnostic/prognostic valueElevated in MCI-AD and AD dementia; discriminate AD from non-AD with AUCs ≥0.80 (SNAP-25aa40 up to AUC 0.93)

LimitationsRequire prospective multi-center validation and standardized assays before routine clinical use

Actigraphy

MethodActigraphy (rest-activity rhythm analysis)

FindingCircadian rhythm fragmentation associated with aging and pre-clinical amyloid pathology in cross-sectional studies

StatusEmerging research biomarker requiring replication and control for sleep disorders/medications

DNA methylation profiling

MethodDNA methylation profiling of CpG sites in peripheral blood or brain tissue

PurposeIdentify differential methylation associated with aging or AD and potential epigenetic biomarkers

EvidenceGenome-wide studies have identified differentially methylated regions but further validation needed

MindX Blood Test

TestMindX Blood Test — mRNA gene expression panel of 24 genes (whole blood)

AvailabilityProprietary, prescription-only test that generates a predictive risk score for memory/AD

Intended useReported for middle-aged or elderly patients with memory complaints; clinical utility not established for routine diagnosis

Discern (NeuroDiagnostics) skin biopsy test

TestDiscern (NeuroDiagnostics) skin biopsy test — cultured skin fibroblasts assessed with AD-Index, morphometric imaging, and PKCε assays

Specimen requirementsPunch skin biopsy cultured for weeks to reach required cell volumes before assays

Regulatory/availabilityProprietary vendor test available by prescription; clinical value for monitoring therapy not established

p-tau231 (plasma)

AnalytePlasma p-tau231

Diagnostic accuracyUltrasensitive Simoa assay distinguished AD from controls with AUC 0.92–0.94 across cohorts

Temporal dynamicsMay increase earlier than other p-tau isoforms relative to amyloid PET positivity

NfL

AnalyteNeurofilament light chain (NfL) — serum/plasma

InterpretationMarker of neurodegeneration that increases prior to symptom onset in familial AD but is not specific to AD

LimitationsOverlap with other neurologic conditions limits use as standalone diagnostic test

GFAP

AnalyteGlial fibrillary acidic protein (GFAP) — plasma/CSF

PerformancePlasma GFAP discriminated Aβ-positive vs Aβ-negative individuals with AUC 0.69–0.86; increases early in AD continuum

LimitationsCross-sectional findings require longitudinal validation

Vessel density (VD) / FAZ / SCP / DCP

MeasuresOCTA-derived metrics: vessel density (VD), foveal avascular zone (FAZ), superficial capillary plexus (SCP), deep capillary plexus (DCP)

FindingsMeta-analyses show decreased VD and changes in FAZ in MCI/AD versus controls, but evidence limited by small, cross-sectional studies

StatusInvestigational for routine diagnostic use pending longitudinal validation and standardized measurement

Automated computerized cognitive assessment aids

Tool typeAutomated computerized cognitive assessment aids (FDA 510(k) cleared)

RoleCleared as adjunctive tools to assess memory and cognitive domains; validated in trials as adjuncts, not replacements for full neuropsychological assessment

Use recommendationConsider as adjunct prior to advanced biomarker testing or in monitoring cognitive outcomes

Clinical Policy Bulletins (metadata)

Document typeClinical Policy Bulletin (CPB) — Alzheimer's Disease Tests, Aetna Policy #0349

Last review date09/08/2023

Next review date04/11/2024

OpenPayer

Alzheimer's Disease Tests

Coverage Criteria and Evidence Summaries

Coding and Billing Guidance

Provider Responsibilities, Prior Authorization, and Documentation

Definitions and Key Terms