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Radiodiagnosis · Neuroimaging

Alzheimer's disease

Morbus Alzheimer

Alzheimer's disease is the leading cause of neurodegenerative dementia, requiring careful neuroimaging analysis. In modern diagnostics, assessing cortical atrophy patterns and identifying concomitant vascular lesions are of paramount importance.

Atrophy scaleA score of "2" is considered pathological up to age 75, and a score of "3" for age over 75.
Risk factorThe combination of cerebral infarcts and Alzheimer's features is the strongest predictor of dementia.
FTLD geneticsOften associated with chromosome 17, mutations in the tau protein gene (MAPT) or progranulin.
4 min readFor medical studentsUpdated Sep 20, 2026
Material prepared by WhiteCoat Pro editorial team based on platform study guidesReviewed by medical editor: Aulov A. A., general practitioner · 09/24/2026

Evaluation of atrophy and atypical forms

In classical diagnostic imaging of Alzheimer's disease (Morbus Alzheimer), the severity of the disease correlates with the degree of brain tissue volume loss. Special atrophy grading scales are used to objectify this, where the significance of the scores depends on the patient's age: a score of "2" indicates pathology in individuals under 75, and a score of "3" in individuals over 75.

Alzheimer's disease in young patients has a distinct diagnostic pattern. In this age group, the hippocampus may remain completely intact (minimal atrophy), making diagnosis by classical criteria difficult. Pathological changes and volume loss dominate in the parietal cortex and precuneus, including the posterior cingulate cortex.

If tomograms reveal pronounced asymmetry of atrophic changes between the left and right hemispheres, the diagnosis of Alzheimer's disease is called into question. In such cases, frontotemporal dementia is suspected first.

Impact of vascular changes

In elderly patients, Alzheimer's disease is frequently accompanied by cerebrovascular pathology. Atherosclerosis causes ischemic damage to brain tissue, which dramatically accelerates the development of specific neurodegenerative pathology.

It is important to note that the combination of cerebral infarcts and morphological signs of Alzheimer's disease is the most powerful predictor of severe dementia development. Vascular changes (primarily white matter lesions visualized on MRI) act as an independent target for therapeutic intervention. Adequate management of vascular risk factors can significantly slow the progression of cognitive decline.

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Frontotemporal lobar degeneration (FTLD)

This is a group of diseases based on tau pathology, manifesting as prominent speech and behavioral disorders. FTLD ranks third in frequency among degenerative dementias (5–10% of all cases) and second among young patients.

The main radiological sign of FTLD is atrophy of the temporal and frontal lobes, which initially is often asymmetric in nature. Speech and behavioral disorders can also occur in atypical Alzheimer's disease, corticobasal degeneration (CBD), and progressive supranuclear palsy (PSP).

According to the Lund–Manchester criteria, 3 main subtypes are distinguished:

  1. Behavioral variant (bvFTD) — at the time of symptom onset, frontal lobe atrophy may be mild.
  2. Non-fluent variant progressive primary aphasia (nfvPPA).
  3. Semantic dementia (SD) — characterized by severe atrophy of the left temporal lobe, with the temporal pole suffering significantly more than the hippocampus. Multi-slice CT is comparable in quality to MRI in demonstrating this focal atrophy.

A significant proportion of cases have an autosomal dominant inheritance pattern. Functional methods (FDG-PET and perfusion MRI) are actively used for the differential diagnosis of FTLD from depression and for detecting early changes. With right-sided lesions, patients often suffer from prosopagnosia (inability to recognize faces).

Vascular dementia (VaD)

Vascular dementia is the second most common type after Alzheimer's disease, and in elderly individuals, both pathologies frequently coexist and mutually exacerbate each other. A strict diagnosis of VaD implies that dementia is secondary exclusively to cerebrovascular disease.

Among pathomorphological variants associated with small and large vessel disease, the following are distinguished:

  • Age-related diffuse confluent white matter changes (ARWMC) / subcortical arteriosclerotic encephalopathy (SAE).
  • Multi-infarct state.
  • Multiple territorial infarcts.
  • Strategic cortico-subcortical infarcts or borderzone infarcts.
  • Cortical laminar necrosis.
  • Delayed post-ischemic demyelination and hippocampal sclerosis.

The mere presence of vascular foci on CT or MRI does not mean the development of dementia. Strict clinical and radiological NINDS-AIREN criteria are applied to confirm the diagnosis.

How to memorize

In young patients with Alzheimer's, atrophy is localized posteriorly (precuneus), and the hippocampus is spared. In semantic dementia (FTLD), atrophy is localized anteriorly (the left temporal pole suffers more than the hippocampus).

Class and exam questions

What does Alzheimer's disease look like in young patients on MRI?

Unlike the classical picture, in young patients the hippocampus may remain intact. Pathological atrophy dominates in the parietal cortex, precuneus, and posterior cingulate cortex.

Do vascular changes on MRI always indicate vascular dementia?

No. Not every vascular pathology is sufficient for the development of dementia. For an accurate diagnosis, strict NINDS-AIREN criteria are applied, taking into account the localization and volume of the lesion.

In which pathology does prosopagnosia occur?

Difficulty recognizing faces (prosopagnosia) is characteristic of frontotemporal lobar degeneration (FTLD) with predominant right-hemisphere involvement.

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What else to study on this topic

  • NINDS-AIREN criteria for the diagnosis of vascular dementia
  • Methodology of FDG-PET and perfusion MRI in FTLD
  • Genetics of dementias: the role of MAPT and progranulin mutations
  • Differential diagnosis of bvFTD and pseudodementia in depression

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