Biochemical dysfunction and memory loss: the case of Alzheimer's dementia

E V Roloff, B Platt

Research output: Contribution to journalLiterature review

30 Citations (Scopus)

Abstract

Among the different types of cognitive impairment that appear with increasing age, Alzheimer's disease (AD) is rated as the most frequent. Despite intensive research, key questions concerning AD aetiology remain elusive, but it appears that many biochemical events crucial for neuronal communication and synaptic plasticity fail during the course of the disease. The aim of this review is therefore to provide an overview of intracellular cascades involved in AD pathology. For almost all factors, it is a matter of controversy whether their contribution should be considered to be cause or effect. However: intracellular signalling may be crucial-as it is in learning and memory mechanisms-and malfunction of biochemical pathways may be a common denominator in neurodegenerative processes, thus providing new venues for treatment and therapeutic strategies.

Original languageEnglish
Pages (from-to)601-616
Number of pages16
JournalCellular and Molecular Life Sciences
Volume55
Issue number4
DOIs
Publication statusPublished - 1999

Keywords

  • Alzheimer
  • acetylcholine
  • beta-amyloid
  • tau
  • Ca2+ homeostasis
  • oxidative stress
  • neurodegeneration
  • second messengers
  • phosphatases
  • kinases
  • AMYLOID PRECURSOR PROTEIN
  • ABNORMALLY PHOSPHORYLATED-TAU
  • POSTMORTEM HUMAN BRAIN
  • NICOTINIC ACETYLCHOLINE-RECEPTORS
  • ADENYLYL-CYCLASE ACTIVITY
  • PAIRED HELICAL FILAMENTS
  • KINASE-C-ALPHA
  • BETA-PROTEIN
  • SIGNAL-TRANSDUCTION
  • PHOSPHOLIPASE-C

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