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Special Issue "Role of Tau Protein in Synaptic Deteriorarion of Alzheimer's Disease (AD)"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: 31 July 2021.

Special Issue Editor

Dr. Giuseppina Amadoro
E-Mail Website
Guest Editor
1. Institute of Translational Pharmacology (IFT)-CNR, Via Fosso del Cavaliere 100, 00133 Rome, Italy
2. European Brain Research Institute (EBRI), Viale Regina Elena 295, 00161 Rome, Italy
Interests: tau protein; Alzheimer's disease (AD); amyloid beta; Amyloid Precursor Protein (APP); synapse; non-AD tauopathies; neurodegeneration

Special Issue Information

Dear Colleagues,

Accumulating evidence suggests that degeneration of synaptic connections is the strongest pathological correlate of cognitive decline in Alzheimer's disease (AD), an age-related neurodegenerative disorder characterized by amyloid beta (Aβ) and tau protein deposition inhibiting the synaptic plasticity of neurons. Experimental studies also indicate that tau pathology—much more strongly than Ab pathology–is the actual driver of synaptic loss and neurodegeneration in AD progression. Accumulation of soluble oligomeric species of tau leads to synaptic degeneration and memory or learning impairment in animal models, regardless of aggregation in neurofibrillary tangles (NFTs). Tau can either directly or indirectly impact synapses and alter neurotransmission by acting both on the pre- and post-synaptic sides, or on either side alone. Targeting of pathological tau restores deficits in synaptic plasticity and attenuates synaptic loss in transgenic mice, opening novel opportunities for an efficacy cure for AD in the face of disappointing Aβ-directed clinical trials. The spread of tau pathology occurs via synaptic connections, indicating that reductions in tau levels will also halt the propagation of the disease throughout the brain. Understanding the physiopathological role of tau in the synapses is crucial for the future development of therapeutic strategies aimed at preventing or reducing the progressive deterioration in cognition and brain function associated with AD pathogenesis. This Special Issue will be focused on recent advances in addressing the emerging role of tau dysmetabolism in synaptic failure in AD and its translational implications.

Dr. Giuseppina Amadoro
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.


  • Tau protein
  • Alzheimer’s disease
  • Synaptotoxicity
  • Neurodegeneration
  • Therapeutic intervention

Published Papers

This special issue is now open for submission.
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