Exploring ageing as a potential new therapeutic target for schizophrenia.

Genetic and environmental risk factors of Parkinsonism

Parkinsonian disorders comprise a broad spectrum of neurodegenerative diseases with a wide variety of pathogenetic processes. These processes lead to the formation of pathological proteins, resulting in the brain diseases called synucleinopathies, tauopathies or TDP-43 proteinopathies. There is currently growing support for the hypothesis that genetic variants explain a significant fraction of the etiology of apparently sporadic parkinsonian disorders. Genetic risk factors can be stratified according to the metabolic or structural processes that can lead to cellular disturbance; these processes involve protein aggregation, protein and membrane trafficking, stabilization of the neurite structure, prion-like transmission of pathological proteins, ubiquitin–proteasome system balance, mitophagy, lysosome autophagy, synaptic functions, and dopamine transmission. Regarding the environmental risk factors, 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. The most important and most frequently studied are pesticides and trichlorethylene. Beside the globally ubiquitous substances which are supposedly neurotoxic and exposure to which can cause manifestations of Parkinsonism, there are more geographically (regionally) specific substances, which cause (or quite recently caused) the manifestation of endemically present Parkinsonism. Among ten types of endemic Parkinsonism, three of them are thought to have an environmental cause: Western Pacific Parkinsonism, Caribbean Parkinsonism, and North France cluster of atypical Parkinsonism.

Epigenetic aging in Alzheimer's disease: Relation to proteome

Alzheimer's disease (AD) arises from heterogeneous biological processes, and long‐term environmental exposures may become biologically embedded, as reflected in epigenetic clocks.

Parkinson's gene linked to early dysfunction in brain cells

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

Simple Summary This article reviews the conserved mechanisms underlying the occurrence of three neurodegenerative diseases across species, with a focus on major studies involving three invertebrate models. It highlights the research history, key milestones, critical aspects, and significant achievements related to neurodegenerative diseases in these models, aiming to identify potential insights for future research on neurodegenerative diseases from various perspectives.

Epigenetic Mechanisms Underlying Cognitive Dysfunction in Parkinson's Disease: Current Evidence and Future Prospects

Epigenetics studies inheritable characteristics and lasting cellular changes that occur without alterations in the DNA sequence. This field is crucial for understanding how environmental factors interact with genes to influence memory, learning, and cognition. In the context of neurodegenerative disorders, particularly Parkinson's disease (PD), epigenetic mechanisms may help explain the molecular basis of cognitive impairment. The purpose of this review is to explore how epigenetic alterations affect gene expression and their potential role in cognitive dysfunction associated with PD.

Elucidating the neuropathological and molecular heterogeneity of amyloid beta and tau in Alzheimer's disease through machine learning and transcriptomic integration

Functional brain network alterations associated with Alzheimer's disease (AD) pathology, including amyloid beta (Aβ) and phosphorylated tau (p‐tau), are difficult to interpret due to overlapping aging‐associated and non‐amyloid biological processes.