Article
Neurosciences
Shu-Yu Liang, Zuo-Teng Wang, Lan Tan, Jin-Tai Yu
Summary: This article introduces the function and dysfunction of microtubule-associated protein tau in the central nervous system and discusses its role in neurodegenerative diseases, tau phosphorylation-related enzymes and proteins, and its relationship with cell dysfunction. The study of tau neurotoxicity provides new directions for the treatment of tauopathies.
MOLECULAR NEUROBIOLOGY
(2022)
Article
Clinical Neurology
Fernando Gonzalez-Ortiz, Michael Turton, Przemyslaw R. Kac, Denis Smirnov, Enrico Premi, Roberta Ghidoni, Luisa Benussi, Valentina Cantoni, Claudia Saraceno, Jasmine Rivolta, Nicholas J. Ashton, Barbara Borroni, Douglas Galasko, Peter Harrison, Henrik Zetterberg, Kaj Blennow, Thomas K. Karikari
Summary: Blood-based biomarkers for amyloid beta and phosphorylated tau show good diagnostic accuracies and agreements with their corresponding CSF and neuroimaging biomarkers, while the blood-based neurodegeneration marker neurofilament light is not specific to Alzheimer's disease. A newly developed blood-based assay for brain-derived tau has shown equivalent diagnostic performance as CSF total-tau, accurately distinguishing Alzheimer's disease from other neurodegenerative diseases.
Article
Biochemistry & Molecular Biology
Marta Jorge-Oliva, Jan R. T. van Weering, Wiep Scheper
Summary: Tau aggregation plays a central role in the pathogenesis of tauopathies, but the response of neurons to tau pathology and the mechanisms leading to neurodegeneration are still unclear. This study investigated the accumulation of granulovacuolar degeneration bodies (GVBs), lysosomal structures that respond to tau pathology, in different tau aggregation models in primary neurons. The results showed that the structure and subcellular localization of tau aggregates may be important factors affecting GVB accumulation. The findings provide insights into the relationship between tau pathology and neurodegeneration.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2023)
Review
Geriatrics & Gerontology
Allie N. N. Greene, Matia B. B. Solomon, Lisa M. Privette M. Vinnedge
Summary: Alzheimer's disease and age-related dementias have a significant impact on individuals and their social networks, but the molecular and genetic causes of late-onset Alzheimer's disease are still unknown. Treatment options are limited, necessitating the exploration of new molecular mechanisms for intervention. This study summarizes the current understanding of Alzheimer's disease pathogenesis and highlights a potential molecular driver, the DEK protein, and its associations with cellular and molecular hallmarks of the disease.
FRONTIERS IN AGING NEUROSCIENCE
(2022)
Review
Neurosciences
Urmi Sengupta, Rakez Kayed
Summary: This review summarizes the histopathological features of specific protein aggregation in several neurodegenerative diseases and discusses their overlap. It also highlights the synergistic interplay among Aβ, tau, and alpha-Syn in these diseases, suggesting a protein triumvirate.
PROGRESS IN NEUROBIOLOGY
(2022)
Article
Agriculture, Dairy & Animal Science
Laura Vidal-Palencia, Cristina Font, Agustin Rebollada-Merino, Gabriel Santpere, Pol Andres-Benito, Isidro Ferrer, Marti Pumarola
Summary: Tauopathies are neurodegenerative diseases characterized by the accumulation of tau protein in cells. This study reports the first case of primary tauopathy in a cat, providing insights into the disease's clinical and pathological features.
Article
Medicine, General & Internal
Christopher Kaufer, Cara S. Schreiber, Anna-Sophia Hartke, Ivo Denden, Stephanie Stanelle-Bertram, Sebastian Beck, Nancy Mounogou Kouassi, Georg Beythien, Kathrin Becker, Tom Schreiner, Berfin Schaumburg, Andreas Beineke, Wolfgang Baumgaertner, Gulsah Gabriel, Franziska Richter
Summary: This study found that even after viral clearance, inflammatory responses and abnormal protein accumulation can occur in the brain, which may contribute to the neurological dysfunction observed in post-COVID-19 syndrome.
Article
Neurosciences
Kayo Yukawa, Satomi Yamamoto-Mcguire, Louis Cafaro, Christine Hong, Fredrik Kamme, Tsuneya Ikezu, Seiko Ikezu
Summary: TTBK1 is an attractive therapeutic target in the early stages of AD, as it can delay the progression of tau pathology by suppressing the expression of phosphorylated tau.
ACTA NEUROPATHOLOGICA COMMUNICATIONS
(2023)
Review
Neurosciences
Narendran Annadurai, Juan B. De Sanctis, Marian Hajduch, Viswanath Das
Summary: The spread of tau pathology in AD mainly occurs through a prion-like manner between cells. The secretion pathway of tau involves unconventional secretory pathways, such as non-vesicular and vesicular mechanisms, leading to tau release into the extracellular space. Further research is needed to understand these pathways for the development of therapeutic approaches targeting prion-like tau forms in AD.
EXPERIMENTAL NEUROLOGY
(2021)
Review
Clinical Neurology
Yingying Zhao, Kamil Kuca, Wenda Wu, Xu Wang, Eugenie Nepovimova, Kamil Musilek, Qinghua Wu
Summary: The JNK signaling pathway is hypothesized to be a potential therapeutic target for neurodegenerative diseases, with sustained activation leading to synaptic dysfunction and neuronal apoptosis. JNK phosphorylates amyloid precursor protein and tau, ultimately resulting in the formation of senile plaques and neurofibrillary tangles.
ALZHEIMERS & DEMENTIA
(2022)
Review
Cell Biology
Huiqin Zhang, Yu Cao, Lina Ma, Yun Wei, Hao Li
Summary: Tau protein binds to microtubules to promote assembly and stability, but loses this ability in tauopathies, leading to pathological changes like AD. Evidence suggests that tauopathies can spread between cells or connected regions. The complex process involves multiple steps including secretion, cellular uptake, transcellular transfer, and seeding, but the exact mechanisms of tau pathology propagation remain unclear.
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
(2021)
Review
Biochemistry & Molecular Biology
Jiaxin Hu, Wenchi Sha, Shuangshuang Yuan, Jiarui Wu, Yunpeng Huang
Summary: This review summarizes the concepts of tau protein aggregation and discusses views on tau protein transmission and toxicity.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2023)
Review
Biochemistry & Molecular Biology
George A. Carlson, Stanley B. Prusiner
Summary: This article discusses the historical research on diseases caused by PrP misfolding and the core features of NDs found later. The discovery that familial prion diseases can be caused by mutations in PrP was important for understanding prion replication and disease susceptibility. Diseases caused by misfolding and aggregation of various proteins can be classified as prion diseases.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2021)
Article
Neurosciences
Zuha Waheed, Jawaria Choudhary, Faria Hasan Jatala, Aneeqa Noor, Inga Zerr, Saima Zafar
Summary: Tau is a microtubule-associated binding protein in the nervous system that stabilizes microtubules in nerve cells. It accumulates as aggregates and tangles, leading to various pathologies. Different splice variants of tau are expressed in the brain and contribute to neurodegenerative diseases. The isoforms have different roles and undergo post-translational modifications at different rates, affecting their physiological and pathological attributes. This article aims to review the roles of tau isoforms and their underlying mechanisms in neurological deficits.
MOLECULAR NEUROBIOLOGY
(2023)
Article
Neurosciences
Sharanjot Kaur, Harkomal Verma, Monisha Dhiman, Gianluca Tell, Gian Luigi Gigli, Francesco Janes, Anil K. Mantha
Summary: Alzheimer's disease is the most common neurodegenerative disease, with pathology involving factors such as Aβ, NFT, oxidative stress, cellular senescence, and inflammation. Exosomes play a role in modulating interactions between cells, transmitting signals that can either benefit or harm neuron function in AD. The field of exosome research in neurodegenerative diseases, especially in Alzheimer's disease, is still in its early stages, with potential for further exploration of their roles.
MOLECULAR NEUROBIOLOGY
(2021)