Neuronal response in Alzheimer's and Parkinson's disease: the effect of toxic proteins on intracellular pathways

Shohreh Majd, John Power, Hugh Grantham

    Research output: Contribution to journalReview articlepeer-review

    42 Citations (Scopus)


    Accumulation of protein aggregates is the leading cause of cellular dysfunction in neurodegenerative disorders. Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease, Prion disease and motor disorders such as amyotrophic lateral sclerosis, present with a similar pattern of progressive neuronal death, nervous system deterioration and cognitive impairment. The common characteristic is an unusual misfolding of proteins which is believed to cause protein deposition and trigger degenerative signals in the neurons. A similar clinical presentation seen in many neurodegenerative disorders suggests the possibility of shared neuronal responses in different disorders. Despite the difference in core elements of deposits in each neurodegenerative disorder, the cascade of neuronal reactions such as activation of glycogen synthase kinase-3 beta, mitogen-activated protein kinases, cell cycle re-entry and oxidative stress leading to a progressive neurodegeneration are surprisingly similar. This review focuses on protein toxicity in two neurodegenerative diseases, AD and PD. We reviewed the activated mechanisms of neurotoxicity in response to misfolded beta-amyloid and aα-synuclein, two major toxic proteins in AD and PD, leading to neuronal apoptosis. The interaction between the proteins in producing an overlapping pathological pattern will be also discussed.

    Original languageEnglish
    Article number69
    Number of pages13
    JournalBMC Neuroscience
    Issue number1
    Publication statusPublished - 23 Oct 2015


    • Alpha-synuclein
    • Alzheimer's disease
    • Beta-amyloid
    • Intracellular signalling
    • Neurodegeneration
    • Neurotoxicity
    • Parkinson's disease


    Dive into the research topics of 'Neuronal response in Alzheimer's and Parkinson's disease: the effect of toxic proteins on intracellular pathways'. Together they form a unique fingerprint.

    Cite this