Revealing the Mechanisms of Alzheimer’s, Parkinson’s and Huntington’s Diseases Through Invertebrate Models

Genetic and environmental risk factors of Parkinsonism

There are several substances that have been supposed of being a risk for the development of neurodegenerative proteinopathy and Parkinsonism, mainly the agents used in agriculture and the textile industry and the environmental risk factors.

Unraveling Neurodegeneration: Common Molecular Mechanisms and Novel Therapeutic Concepts in Major Neurodegenerative Disorders

This review sought to integrate disease‐specific causative triggers with shared pathogenic pathways, focusing on neuroinflammatory signaling, oxidative imbalance, mitochondrial impairment, and disrupted protein homeostasis, in order to support multi‐target, disease‐modifying therapeutic strategies.

Rethinking single-pathology therapies by targeting inflammation and co-pathologies in Parkinson’s disease

Co-expression of tau and amyloid-beta with α-syn pathology is shown in over 50% of Parkinson’s Disease postmortem brains, and these patients present with enhanced cognitive decline and disease phenotype. This review integrates the known immune response in PD with co-pathology incidence, highlighting synergistic interactions between α-syn, tau and Aβ and how this promotes a distinct neuroinflammatory response leading to severe neuronal loss and cognitive symptoms. Based on this, we support the need for combinatorial therapeutic strategies to address this debilitating, yet common factor of disease.

Exploring ageing as a potential new therapeutic target for schizophrenia.

Increased age-related biological changes have been causally linked to various pathologies in the brain, including Alzheimer's and Parkinson's diseases. There is also evidence that schizophrenia could be included in this group of brain disorders that may actually be manifestations of a broader multisystemic premature ageing phenotype.

Elucidating the mechanisms underlying Alzheimer's disease-Elucidating the mechanisms underlying Alzheimer's disease-associated genetic polymorphisms associated genetic polymorphisms

Co- and multipathologies need serious consideration for understanding Parkinson's disease pathogenesis and designing novel experimental therapeutic strategies

Parkinson ’ s disease (PD) is pathologically de fi ned by the presence of aggregated α -synuclein in the form of Lewy bodies and Lewy neurites. 1 – 4 Considerable interest has focused on anti-α -synuclein immunotherapy as a potential disease-modifying strategy for PD, but initial phase 2a clinical trials examining this approach did not meet their primary endpoint. Most recently, the phase 2b PADOVA trial of prasinezumab, published in The Lancet Neurology , also did not meet its primary endpoint, although a non-signi fi cant delay in motor progression and prespeci fi ed exploratory fi ndings suggested potential clinical activity. 5 – 7