Special Issue "Role of Tau Protein in Synaptic Deteriorarion of Alzheimer's Disease (AD)"
Deadline for manuscript submissions: 31 July 2021.
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
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
Manuscript Submission Information
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- Tau protein
- Alzheimer’s disease
- Therapeutic intervention