Non-demented individuals with Alzheimer’s disease neuropathology

Resistance to cognitive decline may reveal new treatment strategies

Research output: Contribution to journalReview article

7 Citations (Scopus)

Abstract

Alzheimer’s disease (AD) is a terminal neurodegenerative disorder that is characterized by accumulation of amyloid plaques and neurofibrillary tangles in the central nervous system. However, certain individuals remain cognitively intact despite manifestation of substantial plaques and tangles consistent with what would be normally associated with fully symptomatic AD. Mechanisms that allow these subjects to escape dementia remain unresolved and understanding such protective biological processes could reveal novel targets for the development of effective treatments for AD. In this review article we discuss potential compensatory mechanisms that allow these individuals to remain cognitively intact despite the typical AD neuropathology.

Original languageEnglish (US)
Pages (from-to)4063-4068
Number of pages6
JournalCurrent Pharmaceutical Design
Volume22
Issue number26
DOIs
StatePublished - Jul 1 2016

Fingerprint

Disease Resistance
Alzheimer Disease
Biological Phenomena
Neurofibrillary Tangles
Amyloid Plaques
Neurodegenerative Diseases
Dementia
Central Nervous System
Neuropathology
Cognitive Dysfunction

Keywords

  • Alzheimer’s disease
  • Compensatory mechanisms in AD
  • Non-demented with Alzheimer’s Neuropathology
  • Resistance to cognitive decline

ASJC Scopus subject areas

  • Pharmacology
  • Drug Discovery

Cite this

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title = "Non-demented individuals with Alzheimer’s disease neuropathology: Resistance to cognitive decline may reveal new treatment strategies",
abstract = "Alzheimer’s disease (AD) is a terminal neurodegenerative disorder that is characterized by accumulation of amyloid plaques and neurofibrillary tangles in the central nervous system. However, certain individuals remain cognitively intact despite manifestation of substantial plaques and tangles consistent with what would be normally associated with fully symptomatic AD. Mechanisms that allow these subjects to escape dementia remain unresolved and understanding such protective biological processes could reveal novel targets for the development of effective treatments for AD. In this review article we discuss potential compensatory mechanisms that allow these individuals to remain cognitively intact despite the typical AD neuropathology.",
keywords = "Alzheimer’s disease, Compensatory mechanisms in AD, Non-demented with Alzheimer’s Neuropathology, Resistance to cognitive decline",
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N2 - Alzheimer’s disease (AD) is a terminal neurodegenerative disorder that is characterized by accumulation of amyloid plaques and neurofibrillary tangles in the central nervous system. However, certain individuals remain cognitively intact despite manifestation of substantial plaques and tangles consistent with what would be normally associated with fully symptomatic AD. Mechanisms that allow these subjects to escape dementia remain unresolved and understanding such protective biological processes could reveal novel targets for the development of effective treatments for AD. In this review article we discuss potential compensatory mechanisms that allow these individuals to remain cognitively intact despite the typical AD neuropathology.

AB - Alzheimer’s disease (AD) is a terminal neurodegenerative disorder that is characterized by accumulation of amyloid plaques and neurofibrillary tangles in the central nervous system. However, certain individuals remain cognitively intact despite manifestation of substantial plaques and tangles consistent with what would be normally associated with fully symptomatic AD. Mechanisms that allow these subjects to escape dementia remain unresolved and understanding such protective biological processes could reveal novel targets for the development of effective treatments for AD. In this review article we discuss potential compensatory mechanisms that allow these individuals to remain cognitively intact despite the typical AD neuropathology.

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