AD is a progressive and relentless disease caused by a continuous underlying process1,2
Changes in AD biomarkers, first Aβ and then tau, precede onset of clinical symptoms3
Adapted from Jack CR Jr, et al, with permission from Elsevier.
AD-related pathophysiological changes in the brain may begin up to 25 years prior to diagnosis, but many patients are diagnosed only after advanced symptom onset4
MCI can be caused by many processes, including cerebrovascular disease and other causes, but more than 60% of cases are due to AD1,5
The earlier MCI due to AD and mild AD dementia are diagnosed and treated, the greater the opportunity for benefit1
Alzheimer’s disease continuum1,6,7
Intervening early can delay progression1,6
Proactive steps to diagnose AD at the earliest symptomatic stages
Check for cognitive impairment8-11
- Patient history/informant observations
- Physical/neurological exams
- While no test represents a gold standard, the following are examples of neurocognitive tools that are sensitive to MCI due to AD and/or mild AD dementia, that can aid in early identification—MoCA, Qmci screen, MMSE, Mini-Cog, SLUMS, and AD8
Rule out non-AD causes8,12,13
- Lab tests can rule out other causes such as vitamin B12 deficiency and thyroid diseases
- Medications/comorbidities could be underlying causes
- CT scans or MRI can rule out other causes such as tumors, evidence of small or large strokes, damage from severe head trauma, or fluid buildup in the brain
Confirm AD diagnosis14,15
- Biomarker-confirmed AD diagnosis allows for Aβ-targeting therapy in appropriate patients
- CSF or PET confirms Aβ pathology
Treatment consideration: ApoE ε4 status16
- Testing for ApoE ε4 status should be performed prior to initiation of treatment with monoclonal antibodies directed against aggregated forms of beta amyloid to inform the risk of developing ARIA
- Prior to testing, prescribers should discuss with patients the risk of ARIA across genotypes and the implications of genetic testing results. Prescribers should inform patients that if genotype testing is not performed, they can still be treated with monoclonal antibodies directed against aggregated forms of beta amyloid