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Alzheimer disease is a chronic, progressive, and irreversible neurodegenerative disorder and the most common cause of dementia in older adults. It leads to gradual neuronal loss, causing cognitive decline, behavioral changes, and loss of functional independence.Risk Factors and EtiologyThe disease is multifactorial. Age is the strongest risk factor, with prevalence doubling every 5 years after age 65. Genetic factors include mutations in genes such as APP, PSEN1, and PSEN2, which are associated...
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Alzheimer disease involves structural changes in the brain that begin long before symptoms appear. The most distinctive features are extracellular neuritic plaques and intracellular neurofibrillary tangles.Neuritic plaques form in the cerebral cortex and around blood vessels. These plaques contain a dense core of beta-amyloid (Aβ)—a toxic protein fragment that clumps outside neurons. The core is surrounded by damaged neuronal extensions, as well as reactive astrocytes and...
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Executive function changes before memory in preclinical Alzheimer's pathology: a prospective, cross-sectional, case

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Area of Science:

  • Neuroscience
  • Neurology
  • Gerontology

Background:

  • Early intervention in Alzheimer's disease (AD) is crucial for mitigating its impact.
  • Focusing on preclinical AD in asymptomatic individuals may reveal earlier disease indicators.
  • While decreased cerebrospinal fluid (CSF) beta-amyloid42 is an early marker, the pathology causing initial clinical effects remains unclear.

Purpose of the Study:

  • To investigate whether neuropsychological changes within the normal range can predict preclinical AD.
  • To identify early pathological markers of AD in asymptomatic individuals.
  • To hypothesize that specific cognitive functions may precede memory impairment in early AD.

Main Methods:

  • Recruited adults with probable AD and cognitively healthy asymptomatic adults.
  • Utilized logistic regression to establish a CSF beta-amyloid42/tau ratio cutoff for AD classification (85% accuracy).
  • Analyzed neuropsychological data, including Stroop Interference, to identify predictors of preclinical AD pathology.

Main Results:

  • Identified a subgroup of asymptomatic individuals with preclinical AD (n=34) based on CSF beta-amyloid42/tau ratios.
  • Stroop Interference (response inhibition) was the sole independent predictor of preclinical AD pathology (OR=0.13).
  • Subgroups with and without preclinical AD showed similar demographics, genetic profiles, and vascular risk factors.

Conclusions:

  • Clinical effects of early amyloid pathology appear to precede hippocampal neurofibrillary pathology.
  • Altered CSF beta-amyloid42 and reduced executive function precede memory impairment in early AD.
  • Stroop Interference shows potential as a screening tool for early AD pathology and for monitoring preclinical AD treatment.