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  • Updated 06.17.2024
  • Expires For CME 06.17.2027

Limbic-predominant age-related TDP-43 encephalopathy (LATE)

Introduction

Overview

It is increasingly clear that a multitude of pathologies (in a population, and within an individual) can underlie the dementia clinical syndrome. Among the most common and impactful of these is limbic-predominant age-related TDP-43 encephalopathy (LATE), a very common “Alzheimer disease mimic” (16). Thus, the symptoms of LATE are similar to those of Alzheimer disease, and the pathology underlying LATE (TDP-43 proteinopathy) commonly, but not inevitably, co-occurs with Alzheimer disease. LATE affects approximately one quarter of individuals over 80 years of age.

Key points

• Limbic-predominant age-related TDP-43 encephalopathy (LATE) is a common condition of aging (affects approximately one quarter of individuals over 80 years old).

• LATE neuropathologic change (LATE-NC) is the pathologic substrate.

• LATE-NC is characterized by TDP-43 pathology, mostly in the medial temporal lobes.

• LATE-NC is often comorbid with Alzheimer disease neuropathologic changes (ADNC, ie, amyloid plaques and neurofibrillary tangles).

• The prevalence of pathologies in persons over the age of 80 are as follows: ADNC+LATE-NC > pure ADNC > pure LATE-NC.

• The severity of the cognitive impairment is as follows: ADNC+LATE-NC > pure ADNC > pure LATE-NC.

Historical note and terminology

TDP-43 proteinopathy is a disease-associated pathological phenomenon discovered by Dr. Manuela Neumann and colleagues at UPENN, in the Drs. John Trojanowski/Virginia Lee CNDR Lab in 2006, in the context of neurologic diseases along a spectrum of frontotemporal lobar degeneration and amyotrophic lateral sclerosis (21). TDP-43 pathology is also associated with over 20 other neurologic diseases (04), with TDPopathies being analogous to tauopathies. This has produced some confusion in the field.

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