Quick Summary

Dementia is a clinical syndrome causing functional decline across cognitive domains. Source pages incomplete or inaccessible — please provide valid URLs: 5 (follow-up).

Alzheimer’s disease is the most common dementia, diagnosed clinically, supported by baseline labs and structural imaging, and managed with symptomatic drugs and individualized psychosocial care.
Warning signs
  • Dangerous aggression or risk of harm needs urgent attention.
  • Violent behavior often requires pharmacologic intervention.
  • Sudden decline or new symptoms require prompt evaluation.

Initial assessment

  • Cognitive decline impairs work and social functioning.
  • Consciousness is usually preserved early.
  • Obtain comprehensive medical and psychiatric history.
  • Include caregiver report of symptoms and behaviors.
  • Perform neuropsychological and neuropsychiatric assessment.
  • Consider memory clinic referral for multidisciplinary care.

Diagnosis

  • Use DSM‑5 to diagnose dementia subtypes.
  • Diagnosis is based on clinical assessment.
  • Alzheimer’s disease is a clinical degenerative syndrome.
  • MRI supportive with hippocampal or global cortical atrophy.
  • DLB shows minimal medial temporal atrophy on MRI.
  • Vascular dementia requires clinical history and imaging evidence.

Diagnostics (Lab Test and Imaging)

  • Baseline labs include CBC, electrolytes, LFTs, renal, glucose, thyroid, B12, folate.
  • Screens for syphilis when clinically suspected.
  • EEG in suspected CJD, seizures, or delirium.
  • Obtain structural brain imaging in all patients.
  • MRI preferred. CT if MRI unavailable or contraindicated.
  • FDG‑PET may aid when diagnosis remains uncertain.

Pharmacological management

  • Cholinesterase inhibitors
    • Indication: all stages of Alzheimer’s disease.
    • Benefits: improve cognition, behavior, function.
    • Use in DLB and Parkinson’s disease dementia.
    • Not for frontotemporal dementia or MCI.
  • Memantine
    • Indication: moderate to severe Alzheimer’s disease.
    • Monotherapy if cholinesterase inhibitor not tolerated.
    • Combination may delay symptom progression.
  • Anti‑amyloid monoclonal antibodies
    • Donanemab for early Alzheimer’s with confirmed amyloid.
    • Lecanemab for MCI due to Alzheimer’s or mild Alzheimer’s.
    • Reduce amyloid plaques in early disease.
  • Antipsychotics for agitation or psychosis
    • Reserve for severe distress or dangerous aggression.
    • Use lowest effective dose for shortest time.
    • Reassess at least every six weeks.
    • Consider taper within sixteen weeks when possible.
  • Benzodiazepines
    • Use only when necessary for anxiety or procedures.
    • Start low and titrate cautiously.
    • Prefer short‑acting or non‑metabolized agents.
  • Antidepressants
    • SSRIs are preferred for depression in Alzheimer’s.
    • Consider venlafaxine or mirtazapine.
    • Start low and increase carefully.

Follow up / Monitoring

  • Assess disease severity before starting medications.
  • Monitor cognitive, behavioral, and functional outcomes.
  • Titrate or switch therapy based on response.
  • Reassess antipsychotics at least every six weeks.
  • Taper antipsychotics within sixteen weeks when feasible.
  • Educate patients and caregivers on routine follow‑up.

Special situations

  • Early‑onset familial Alzheimer’s due to APP, PSEN1, PSEN2.
  • Down syndrome increases risk of irreversible dementia.
  • DLB features parkinsonism and visual hallucinations.
  • DLB has neuroleptic sensitivity risk.
  • PDD shows dementia years after motor symptoms.
  • FTD presents with early behavioral and language change.

Overview

Dementia and Alzheimer’s Disease are terms that are usually interchanged. In the Introduction section, this will be clarified.

There are millions of people affected by Alzheimer’s disease regionally and worldwide. Details on the number of individuals affected are in the Epidemiology section.

There are many causes of Alzheimer’s disease. The Etiology section enumerated these causes. The complex and multifactorial pathophysiology of Alzheimer’s disease is discussed in the Pathophysiology section.

The modifiable and non-modifiable risk factors of Alzheimer’s disease are enumerated in the Risk Factors section, while the different types of Alzheimer’s disease are discussed in the Classification section. 

History and Physical Examination

The Clinical Presentation and History sections detail the cognitive and other manifestations of Alzheimer's disease. The Physical Examination section mentions the neurologic assessment needed to rule out treatable causes of the disease.

Diagnosis

Diagnostic criteria in diagnosing Alzheimer's disease are in the Diagnosis or Diagnostic Criteria section.

The Screening, Laboratory Tests and Ancillaries and Imaging sections enumerate the tests that can be performed in assessing and evaluating the effect of the disease on the patient.

Other diseases to be considered which present similarly are in the Differential Diagnosis section.

Management

There are several drugs that can be considered in the management of cognitive and neuropsychiatric symptoms of Alzheimer’s disease and they are enumerated and discussed in the Pharmacological Therapy section.

Several supportive measures and psychotherapies can be given to patients with Alzheimer’s disease and the Nonpharmacological section explains each one.

The Prevention section enumerates the ways to prevent the disease through the modifiable risk factors identified. 

Frequently Asked Questions

What early features suggest Alzheimer’s disease clinically?
Insidious onset and progressive decline with prominent short-term memory loss is typical. Subsequent impairments involve executive function, language, visuospatial skills, personality and behavior, with loss of ADLs. Psychiatric symptoms (depression, apathy, irritability, agitation) are common; seizures and myoclonus occur late. Differentiate from vascular dementia (stepwise), DLB (fluctuations, visual hallucinations), and FTD (early personality/language change) [1]. Clarification: Corroborate with informant history and screen for reversible contributors before assigning etiology. /disease/alzheimers-disease-dementia/disease-background?subsection=classification
Which cognitive screening tools are recommended initially?
Use validated tools: MoCA, 7‑Minute Screen, Memory Impairment Screen, MMSE, Abbreviated Mental Test, and Clock Drawing. Interpret scores considering education, language, culture, literacy, and sensory deficits. Abnormal screens prompt comprehensive assessment; normal screens do not exclude disease if concern remains. Early referral to multidisciplinary memory services supports accurate diagnosis and coordinated care [1]. Clarification: Use the same instrument over time; obtain informant ADL/IADL history and consider neuropsychological testing when screens are normal. /disease/alzheimers-disease-dementia/initial-assessment?subsection=screening
Which baseline tests exclude reversible cognitive decline?
Order CBC, electrolytes, renal and liver panels, glucose, thyroid function, vitamin B12 ± folate, and syphilis serology when indicated. EEG is useful when CJD, seizures, or delirium are suspected. CSF biomarkers, plasma markers, genetic testing, and APOE genotyping are not routinely recommended [1]. Clarification: Tailor additional tests to clinical clues; review medications with anticholinergic or sedative properties, and treat contributory conditions before labeling dementia. /disease/alzheimers-disease-dementia/diagnostics?subsection=laboratory-tests-ancillaries
When should I order neuroimaging, and what?
Obtain structural brain imaging in all new dementia evaluations. MRI without contrast is preferred for early diagnosis and subcortical vascular changes; noncontrast CT is acceptable if MRI is unavailable or contraindicated. In hypertensive cognitive decline, CT/MRI detect silent infarcts, microbleeds, and white‑matter lesions. FDG‑PET may improve accuracy when diagnostic uncertainty persists [1]. Clarification: Choose modality by availability, safety, and the question posed; integrate imaging with clinical findings. /disease/alzheimers-disease-dementia/diagnostics?subsection=imaging
Which medications improve cognition and manage agitation?
Cholinesterase inhibitors (donepezil, rivastigmine, galantamine) improve cognition, behavior, and function; use across stages. Memantine benefits moderate–severe disease or when cholinesterase inhibitors are not tolerated. For early symptomatic disease with confirmed amyloid, consider donanemab or lecanemab. For agitation/psychosis unresponsive to nonpharmacologic measures, use antipsychotics cautiously; benzodiazepines only selectively; SSRIs treat depression [1]. Clarification: Set expectations that benefits are symptomatic; monitor efficacy and adverse effects; use lowest effective dose for the shortest time and reassess regularly. /disease/alzheimers-disease-dementia/management?subsection=pharmacological-therapy