---
title: "Atypical Alzheimer disease: a multi-axis framework to define clinical and biological heterogeneity"
id: "nature-reviews-neurology-0-atypical-alzheimer-disease-a-multi-axis-framework-toward-defining-heterogeneity"
canonical_url: "https://medichelpline.com/clinical-feed/nature-reviews-neurology-0-atypical-alzheimer-disease-a-multi-axis-framework-toward-defining-heterogeneity"
content_type: "clinical_feed_article"
specialty: "Neurology"
source_name: "Nature Reviews Neurology"
source_url: "https://www.nature.com/articles/s41582-026-01267-y"
published_at: "2026-09-18T12:00:00.000Z"
evidence_level: "Journal Feed"
license: "CC-BY-NC-4.0 / Informational Use"
---
# Atypical Alzheimer disease: a multi-axis framework to define clinical and biological heterogeneity
## Provenance & Clinical Metadata
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- **Specialty:** [Neurology](https://medichelpline.com/clinical-feed/neurology.md)
- **Primary Source:** Nature Reviews Neurology
- **Source URL:** [Original Journal Publication](https://www.nature.com/articles/s41582-026-01267-y)
- **Published At:** 2026-09-18T12:00:00.000Z
- **Evidence Rating:** Journal Feed
## Executive GIST (TL;DR)
- Alzheimer disease (AD) is biologically defined by **amyloid-β (Aβ)** plaques and **tau** neurofibrillary tangles, but these pathologies show regional heterogeneity that underlies diverse clinical presentations. - Typical AD commonly presents with memory impairment; **atypical AD** presents with prominent non-memory symptoms such as visual, language, behavioural, executive or motor/praxis deficits. - Recognized atypical syndromes include posterior cortical atrophy, logopenic variant primary progressive aphasia, behavioural/dysexecutive AD and corticobasal syndrome. - Aβ biomarkers generally establish AD biological status; by contrast, regional **tau**, neurodegeneration and dysfunction map more closely to the affected brain networks and presenting symptoms. - Atypical variants often have younger onset than typical AD and serve as human models for studying selective neuronal and circuit vulnerability. - Factors that may modify network topography and progression rate (tempo) include genetic background, co-pathologies and states of immune–glial, vascular, synaptic or protein-handling systems. - Current biomarker frameworks for amyloid, tau and neurodegeneration confirm AD biology but do not fully capture clinical phenotype, network topography or tempo. - The authors propose a practical four-axis framework — clinical phenotype, AD biological context, network topography and tempo — integrating clinical, neuropathological, imaging, genetic and molecular evidence. - This **multi-axis framework** aims to reduce diagnostic mismatches, improve cohort comparability and support clinical trials with outcomes tailored to affected brain networks. - Details on specific study outcomes, numerical data and full methodological descriptions were not reported in the previewed source content.
## Clinical Analysis & Structured Key Points
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[nature](https://www.nature.com/) 2. [nature reviews neurology](https://www.nature.com/nrneurol) 3. [review articles](https://www.nature.com/nrneurol/articles?type=review-article) 4. article * Review Article * Published: 18 September 2026 # Atypical Alzheimer disease: a multi-axis framework toward defining heterogeneity * [Lea T. Grinberg](https://www.nature.com/articles/s41582-026-01267-y#auth-Lea_T_-Grinberg-Aff1-Aff2) [ORCID: orcid.org/0000-0002-6809-0618](https://orcid.org/0000-0002-6809-0618)[1](https://www.nature.com/articles/s41582-026-01267-y#Aff1),[2](https://www.nature.com/articles/s41582-026-01267-y#Aff2) & * [Melissa E. Murray](https://www.nature.com/articles/s41582-026-01267-y#auth-Melissa_E_-Murray-Aff1-Aff2) [ORCID: orcid.org/0000-0001-7379-2545](https://orcid.org/0000-0001-7379-2545)[1](https://www.nature.com/articles/s41582-026-01267-y#Aff1),[2](https://www.nature.com/articles/s41582-026-01267-y#Aff2) [_Nature Reviews Neurology_](https://www.nature.com/nrneurol) (2026) [Cite this article](https://www.nature.com/articles/s41582-026-01267-y#citeas) [ Save article ](https://www.nature.com/articles/s41582-026-01267-y/save-research?_csrf=Q9c-m5uzxtYWpSXIPRJZspx9QbDpmjnI) [ View saved research ](https://www.nature.com/saved-research) ## Abstract Alzheimer disease (AD) is defined biologically by the presence of amyloid-β (Aβ) plaques and tau neurofibrillary tangles in the brain; however, these pathologies do not affect all brain regions equally. Typical AD usually presents with memory impairment, whereas atypical forms of AD, including posterior cortical atrophy, logopenic variant primary progressive aphasia, behavioural and dysexecutive AD, and corticobasal syndrome, manifest with prominent non-memory symptoms. Aβ biomarkers usually confirm that AD pathology is present, whereas regional tau, neurodegeneration and dysfunction more closely track the affected network and the presenting symptoms. The atypical variants, which tend to present at a younger age than typical AD, provide human models to study selective vulnerability of neurons and circuits. They also help us to test whether immune–glial, vascular, protein-handling, synaptic or genetic factors shape regional vulnerability and rate of progression beyond total Aβ and tau burden. In this Review, we integrate clinical, neuropathological, imaging, genetic and molecular evidence to describe atypical AD within the broader AD spectrum. We propose a practical multi-axis framework comprising clinical phenotype, AD biological context (AD pathology plus co-pathologies and molecular modifiers), network topography (regional patterns) and tempo (rate of clinical and biomarker progression). This framework could reduce diagnostic mismatches, make cohorts more comparable and support trials that include outcomes tailored to the affected brain networks. ## Key points * Atypical Alzheimer disease (AD) presents with early visual, language, behavioural, executive and/or motor and praxis symptoms but remains biologically defined by amyloid-β (Aβ) and tau pathology. * Aβ biomarkers usually establish AD biological status but regional tau pathology, neurodegeneration and dysfunction more closely track symptoms and affected brain networks. * Atypical AD variants expose selective vulnerability and relative sparing, helping us to test why specific circuits fail earlier or more severely in some patients. * Younger onset, genetic background, co-pathology, and immune–glial, vascular, synaptic or protein-handling states might modify network topography and rate of disease progression (tempo). * Current amyloid, tau and neurodegeneration biomarker frameworks confirm AD biology but do not fully capture clinical phenotype, affected network or tempo. * A four-axis framework recording clinical phenotype, AD biological context, network topography and tempo could improve diagnosis, cohort design and trial stratification. This is a preview of subscription content, [access via your institution](https://wayf.springernature.com?redirect_uri=https%3A%2F%2Fwww.nature.com%2Farticles%2Fs41582-026-01267-y) ## Access options [ Access through your institution ](https://wayf.springernature.com?redirect_uri=https%3A%2F%2Fwww.nature.com%2Farticles%2Fs41582-026-01267-y) Access Nature and 54 other Nature Portfolio journals Get Nature+, our best-value online-access subscription 27,99 € / 30 days cancel any time [Learn more](https://shop.nature.com/products/plus/?region=ROW) Subscribe to this journal Receive 12 print issues and online access 176,64 € per year only 14,72 € per issue [Learn more](https://www.nature.com/nrneurol/subscribe) Buy this article * Purchase on SpringerLink * Instant access to the full article PDF. 39,95 € Prices may be subject to local taxes which are calculated during checkout ### Additional access options: * [Log in](https://idp.nature.com/authorize/natureuser?client_id=grover&redirect_uri=https%3A%2F%2Fwww.nature.com%2Farticles%2Fs41582-026-01267-y) * [Learn about institutional subscriptions](https://www.springernature.com/gp/librarians/licensing/license-options) * [Read our FAQs](https://support.nature.com/en/support/home) * [Contact customer support](https://www.springernature.com/gp/contact) **Fig. 1: Complementary approaches to NFT topography in AD.** ![](https://media.springernature.com/m312/springer-static/image/art%3A10.1038%2Fs41582-026-01267-y/MediaObjects/41582_2026_1267_Fig1_HTML.png) **Fig. 2: A multi-axis framework for describing AD heterogeneity.** ![](https://media.springernature.com/m312/springer-static/image/art%3A10.1038%2Fs41582-026-01267-y/MediaObjects/41582_2026_1267_Fig2_HTML.png) **Fig. 3: Milestones in atypical AD research.** ![](https://media.springernature.com/m312/springer-static/image/art%3A10.1038%2Fs41582-026-01267-y/MediaObjects/41582_2026_1267_Fig3_HTML.png) ### Explore related subjects Discover the latest articles and news in related subjects. * [Alzheimer's disease](https://www.nature.com/subjects/alzheimers-disease) ## References 1. 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