About this Research Topic
According to the World Health Organization, about 35.6 million persons in the world are reached by dementia. To date, 60-70% of the cases of dementia are attributed to the Alzheimer's disease (AD). AD is a neurodegenerative disorder characterized by a hyperphosphorylation and an aggregation of tau proteins, an aggregation of Aβ peptides associated to a neuronal loss.
In last years, among the new ideas and emerging therapeutic strategies against AD, some are devoted to:
1) Block the tau hyperphosphorylation, by acting directly or indirectly on both tau kinases and/or phosphatases activities via new pharmacological agents;
2) Block the aggregation of tau, by acting on the withdrawals of the tau protein aggregates by stimulation/inhibition of specific tau phosphorylation sites or still the stimulation of the tau glycosylation;
3) Decrease the amount of tau proteins per se;
4) Block the formation of Aβ peptides;
5) Stimulate the elimination processes of the aggregated tau proteins
a. by stimulation of the classic ways of protein degradation such as the autophagic pathway
b. by targeted immunotherapy
Our goal in this Specific Research Topic is to gather experts in the field to will discuss the etiology of AD and the related therapeutic opportunities for the next decade. Research findings, reviews, new insights, new approaches are welcome and may include but are not limited to:
- AD and related tauopathies
- Tau phosphorylation/dephosphorylation (including PP2A, Pin-1 and tau kinases…)
- Tau post-translational modifications
- Pharmacological compounds against AD
- Animal models with AD or related pathology
- Neuroprotection strategies and new therapeutic ways
- AD: a conformational disease?
- Risk factors and protectors
- AD and genetics
In last years, among the new ideas and emerging therapeutic strategies against AD, some are devoted to:
1) Block the tau hyperphosphorylation, by acting directly or indirectly on both tau kinases and/or phosphatases activities via new pharmacological agents;
2) Block the aggregation of tau, by acting on the withdrawals of the tau protein aggregates by stimulation/inhibition of specific tau phosphorylation sites or still the stimulation of the tau glycosylation;
3) Decrease the amount of tau proteins per se;
4) Block the formation of Aβ peptides;
5) Stimulate the elimination processes of the aggregated tau proteins
a. by stimulation of the classic ways of protein degradation such as the autophagic pathway
b. by targeted immunotherapy
Our goal in this Specific Research Topic is to gather experts in the field to will discuss the etiology of AD and the related therapeutic opportunities for the next decade. Research findings, reviews, new insights, new approaches are welcome and may include but are not limited to:
- AD and related tauopathies
- Tau phosphorylation/dephosphorylation (including PP2A, Pin-1 and tau kinases…)
- Tau post-translational modifications
- Pharmacological compounds against AD
- Animal models with AD or related pathology
- Neuroprotection strategies and new therapeutic ways
- AD: a conformational disease?
- Risk factors and protectors
- AD and genetics
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
