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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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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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Dementia is an acquired, progressive syndrome characterized by a decline in multiple cognitive domains severe enough to impair daily functioning and reduce independence. Although memory loss is a central feature, the diagnosis requires additional deficits involving language, executive function, visuospatial skills, judgment, calculation, or abstract reasoning. These cognitive impairments reflect underlying neurodegenerative or vascular processes that gradually disrupt neuronal networks...
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Alzheimer's Disease (AD), a neurodegenerative disorder, is pathologically identified by amyloid plaques and neurofibrillary tangles composed of tau protein. AD pharmacotherapy aims to manage cognitive symptoms, delay disease progression, and treat behavioral symptoms. The treatment is primarily symptomatic and palliative, with no definitive disease-modifying therapy available. Cholinesterase inhibitors, including donepezil (Aricept), rivastigmine (Exelon), and galantamine (Razadyne), are...
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Posterior AD-type pathology: cognitive subtypes emerging from a cluster analysis.

Antonella Cappa1, Nicoletta Ciccarelli2, Eleonora Baldonero2

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Alzheimer's disease (AD) can manifest in various cognitive patterns beyond memory loss. Cluster analysis reveals distinct AD subtypes, including those with visuospatial and language deficits, indicating varied network vulnerability.

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Area of Science:

  • Neuroscience
  • Neurology
  • Cognitive Science

Background:

  • Alzheimer's disease (AD) neuropathology can shift posteriorly, causing posterior cortical atrophy (PCA) with visual deficits.
  • PCA is hypothesized to represent a "dorsal stream" syndrome within AD.

Purpose of the Study:

  • To identify distinct patient subgroups in AD using data-driven cluster analysis of neuropsychological findings.
  • To determine if visuospatial deficits consistent with PCA emerge as a specific subgroup in AD patients.

Main Methods:

  • Principal component analysis of neuropsychological tasks in 23 PCA and 16 DAT patients.
  • Hierarchical cluster analysis performed on five factors: memory, language, perceptual, visuospatial, and calculation.

Main Results:

  • Four distinct clusters of cognitive impairment were identified: visuospatial/perceptual, memory, perceptual/calculation, and language.
  • A clear visuospatial deficit was prominent in only one cluster.

Conclusions:

  • Alzheimer's disease pathology can result in subtypes beyond memory (DAT) and visuospatial (PCA) deficits.
  • Distinct syndromic subtypes with visual perception and language disorders suggest differential vulnerability of functional networks in AD.