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How Many Alzheimer-Perusini's Atypical Forms Do We Still Have to Discover?

Luigi Donato1,2, Domenico Mordà1,2, Concetta Scimone1,2

  • 1Department of Biomedical and Dental Sciences and Morphofunctional Imaging, Division of Medical Biotechnologies and Preventive Medicine, University of Messina, Via Consolare Valeria 1, 98125 Messina, Italy.

Biomedicines
|July 29, 2023
PubMed

Insights

Alzheimer-Perusini's disease, a common dementia, is increasingly understood at a molecular level. Research into atypical variants and neuroinflammation may lead to targeted therapies for this public health challenge.

Area of Science:

  • Neurology
  • Neuroscience
  • Pathology

Background:

  • Alzheimer-Perusini's disease (AD) is the most prevalent dementia worldwide, posing a significant public health concern.
  • Knowledge of AD has evolved from clinical and histopathological descriptions to a deeper molecular understanding, including mixed proteinopathies and altered glial/neuronal phenotypes.

Purpose of the Study:

  • To review recent classifications of atypical Alzheimer-Perusini's disease variants.
  • To summarize clinical evidence for these variants using diagnostic criteria.
  • To discuss molecular-genetic aspects, focusing on neuroinflammation and immune system involvement.

Main Methods:

  • Review of recent classifications of atypical AD variants.
  • Analysis of clinical evidence, including post-mortem neurofibrillary tangle density, cerebral atrophy, and FDG-PET studies.
  • Discussion of molecular-genetic factors, particularly microglial activity and immune system control.

Main Results:

  • Four atypical forms of AD are better defined: posterior cortical atrophy (PCA), logopenic variant of primary progressive aphasia (LvPPA), behavioral/dysexecutive variant, and AD with corticobasal degeneration (CBS).
  • Classifications aid in better defining these variants.
  • Molecular-genetic aspects, including neuroinflammation, are crucial for understanding AD.

Conclusions:

  • Despite advances, no disease-modifying therapies for AD are currently available.
  • Developing specific molecular profiles for individual AD cases is essential for discovering targeted therapies.
  • Understanding atypical variants and neuroinflammatory mechanisms is key to future therapeutic strategies.
Keywords:
amyloid plaquesatypical AD formsgeneticsmicroglianeurofibrillary tangles

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