Joerg Neddens
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View article: Montelukast alleviates neuroinflammation and improves motor functions in the line 61 model of Parkinson's disease: An exploratory study
Montelukast alleviates neuroinflammation and improves motor functions in the line 61 model of Parkinson's disease: An exploratory study Open
Parkinson's disease (PD) is a neurodegenerative movement disorder of high global burden. Uncertainties regarding its exact etiology have been hindering the development of curative therapies. As microglia, the brain's immune cells, are susp…
View article: Cerebral Amyloid Angiopathy like pathology accompanied by intense gliosis in T2D‐induced APPxhQC mice
Cerebral Amyloid Angiopathy like pathology accompanied by intense gliosis in T2D‐induced APPxhQC mice Open
Background Cerebral Amyloid Angiopathy (CAA), characterized by the presence of amyloid β (Aβ) deposits in cerebral blood vessels has been associated with cognitive impairment and Alzheimer’s disease (AD). Vascular risk factors, such as typ…
View article: Motor deficits and brain pathology in the Parkinson’s disease mouse model hA53Ttg
Motor deficits and brain pathology in the Parkinson’s disease mouse model hA53Ttg Open
Background Parkinson’s disease (PD) is a debilitating neurodegenerative disorder characterized by the progressive loss of dopaminergic neurons and the accumulation of α-synuclein (α-syn) aggregates. The A53T missense point mutation occurs …
View article: Sex and genotype dependent differences in amyloid beta levels and lipid metabolism in type 2 diabetic APPxhQC transgenic mice
Sex and genotype dependent differences in amyloid beta levels and lipid metabolism in type 2 diabetic APPxhQC transgenic mice Open
Background Accumulation of amyloid beta (Aβ) and tau proteins have for decades been thought to be central in the pathogenesis of Alzheimer’s disease (AD). More recently, a plethora of evidence emerged that links metabolic dysfunctions such…
View article: Characterization of an APP/tau rat model of Alzheimer’s disease by positron emission tomography and immunofluorescent labeling
Characterization of an APP/tau rat model of Alzheimer’s disease by positron emission tomography and immunofluorescent labeling Open
Background To better understand the etiology and pathomechanisms of Alzheimer’s disease, several transgenic animal models that overexpress human tau or human amyloid-beta (Aβ) have been developed. In the present study, we generated a novel…
View article: Evaluation of Neuropathological Features in the SOD1-G93A Low Copy Number Transgenic Mouse Model of Amyotrophic Lateral Sclerosis
Evaluation of Neuropathological Features in the SOD1-G93A Low Copy Number Transgenic Mouse Model of Amyotrophic Lateral Sclerosis Open
Amyotrophic lateral sclerosis (ALS) still depicts an incurable and devastating disease. Drug development efforts are mostly based on superoxide dismutase 1 gene (SOD1)-G93A mice that present a very strong and early phenotype, allowing only…
View article: Metabolic, Phenotypic, and Neuropathological Characterization of the Tg4-42 Mouse Model for Alzheimer’s Disease
Metabolic, Phenotypic, and Neuropathological Characterization of the Tg4-42 Mouse Model for Alzheimer’s Disease Open
Background: Preclinical Alzheimer’s disease (AD) research strongly depends on transgenic mouse models that display major symptoms of the disease. Although several AD mouse models have been developed representing relevant pathologies, only …
View article: Quantification of Huntington’s Disease Related Markers in the R6/2 Mouse Model
Quantification of Huntington’s Disease Related Markers in the R6/2 Mouse Model Open
Huntington’s disease (HD) is caused by an expansion of CAG triplets in the huntingtin gene, leading to severe neuropathological changes that result in a devasting and lethal phenotype. Neurodegeneration in HD begins in the striatum and spr…
View article: Correlation of Aβ‐pE(3) and ptau in human and mouse brain
Correlation of Aβ‐pE(3) and ptau in human and mouse brain Open
Background Senile plaques frequently contain pyroglutamate amyloid β (Aβ‐pE(3)), a N‐terminally truncated Aβ species that is more closely linked to Alzheimer’s Disease (AD) compared to other Aβ species. Tau protein is highly phosphorylated…
View article: Constant Levels of Tau Phosphorylation in the Brain of htau Mice
Constant Levels of Tau Phosphorylation in the Brain of htau Mice Open
Excessive tau phosphorylation is the hallmark of tauopathies. Today's research thus focusses on the development of drugs targeting this pathological feature. To test new drugs in preclinical studies, animal models are needed that properly …
View article: Correlation of pyroglutamate amyloid β and ptau Ser202/Thr205 levels in Alzheimer’s disease and related murine models
Correlation of pyroglutamate amyloid β and ptau Ser202/Thr205 levels in Alzheimer’s disease and related murine models Open
Senile plaques frequently contain Aβ-pE(3), a N-terminally truncated Aβ species that is more closely linked to AD compared to other Aβ species. Tau protein is highly phosphorylated at several residues in AD, and specifically phosphorylatio…
View article: Transgene integration causes RARB downregulation in homozygous Tg4–42 mice
Transgene integration causes RARB downregulation in homozygous Tg4–42 mice Open
Alzheimer’s disease can be modelled by different transgenic mouse strains. To gain deeper insight into disease model mechanisms, the previously described Tg4–42 mouse was analysed for transgene integration. On RNA/DNA level the transgene i…
View article: Characterization of the visceral and neuronal phenotype of 4L/PS-NA mice modeling Gaucher disease
Characterization of the visceral and neuronal phenotype of 4L/PS-NA mice modeling Gaucher disease Open
Gaucher disease is caused by a deficiency in glucocerebrosidase that can result in non-neuronal as well as neuronal symptoms. Common visceral symptoms are an increased organ size, specifically of the spleen, and glucosylceramide as well as…
View article: P1‐112: PROGRESSIVE INCREASE OF ALZHEIMER'S DISEASE PATHOLOGY IN 5XFAD TRANSGENIC MICE
P1‐112: PROGRESSIVE INCREASE OF ALZHEIMER'S DISEASE PATHOLOGY IN 5XFAD TRANSGENIC MICE Open
Today, Alzheimer's disease (AD) is one of the most devastating neurodegenerative diseases worldwide. Pathologically increased β-amyloid (Aβ) in the brain of AD patients is thought to be one of the main causes for the observed progressive c…
View article: P4‐061: TAU PHOSPHORYLATION PROFILE OF HTAU TRANSGENIC MICE
P4‐061: TAU PHOSPHORYLATION PROFILE OF HTAU TRANSGENIC MICE Open
Alzheimer's disease is characterized by phosphorylation and aggregation of the microtubule associated protein tau. Reliable in vivo models that mimic tau phosphorylation are therefore needed. The hTau transgenic mouse features expression o…
View article: P3‐113: UNTANGLING ALZHEIMER'S DISEASE HALLMARKS IN SENSORY SYSTEMS OF RODENT MODELS
P3‐113: UNTANGLING ALZHEIMER'S DISEASE HALLMARKS IN SENSORY SYSTEMS OF RODENT MODELS Open
Alzheimer's disease (AD) is the most common form of neurodegenerative dementia. Major hallmarks of the disease are: (1) extracellular plaque deposits of the β-amyloid peptide (Aβ) and (2) intracellular neurofibrillary tangles of phosphoryl…
View article: Hepatic and neuronal phenotype of NPC1−/− mice
Hepatic and neuronal phenotype of NPC1−/− mice Open
Niemann-Pick type C disease (NPC) is a fatal autosomal recessive disorder characterized by a defect in the intracellular transport of lipoproteins leading to the accumulation of lipids in diverse tissues. A visceral and neuronal phenotype …
View article: Phosphorylation of different tau sites during progression of Alzheimer’s disease
Phosphorylation of different tau sites during progression of Alzheimer’s disease Open
Alzheimer's disease is characterized by accumulation of amyloid plaques and tau aggregates in several cortical brain regions. Tau phosphorylation causes formation of neurofibrillary tangles and neuropil threads. Phosphorylation at tau Ser2…
View article: mTh1 driven expression of hTDP-43 results in typical ALS/FTLD neuropathological symptoms
mTh1 driven expression of hTDP-43 results in typical ALS/FTLD neuropathological symptoms Open
Transgenic mouse models are indispensable tools to mimic human diseases and analyze the effectiveness of related new drugs. For a long time amyotrophic lateral sclerosis (ALS) research depended on only a few mouse models that exhibit a ver…
View article: Large-Scale Oral Treatment Study with the Four Most Promising D3-Derivatives for the Treatment of Alzheimer’s Disease
Large-Scale Oral Treatment Study with the Four Most Promising D3-Derivatives for the Treatment of Alzheimer’s Disease Open
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder that is associated with the aggregation of the amyloid β protein (Aβ). Aβ oligomers are currently thought to be the major neurotoxic agent responsible for disease develop…
View article: [P1–113]: HUMAN AD AND MOUSE MODELS: PE3‐ABETA AND TAU–ASSOCIATED PATHOLOGY
[P1–113]: HUMAN AD AND MOUSE MODELS: PE3‐ABETA AND TAU–ASSOCIATED PATHOLOGY Open
Alzheimer's disease (AD) is a neurodegenerative disease characterized by extracellular amyloid plaques and intracellular neurofibrillary tangles. Neuritic plaques often appear in N-terminally truncated forms with a cyclic glutamate residue…
View article: [P4–048]: CONCOMITANT EXPRESSION OF INDUCED AAV‐P301L TAU AND TRANSGENIC β‐AMYLOID IN A MOUSE MODEL MIMICKING HUMAN ALZHEIMER's DISEASE
[P4–048]: CONCOMITANT EXPRESSION OF INDUCED AAV‐P301L TAU AND TRANSGENIC β‐AMYLOID IN A MOUSE MODEL MIMICKING HUMAN ALZHEIMER's DISEASE Open
Alzheimer's disease (AD) is an irreversible neurodegenerative process in which memory functions, intellectual abilities and reasoning skills are progressively lost. AD brains are diagnosed under the co-existence of two main pathological ha…
View article: Early start of progressive motor deficits in Line 61 α-synuclein transgenic mice
Early start of progressive motor deficits in Line 61 α-synuclein transgenic mice Open
In summary, our results strengthen and further expand our knowledge about the Line 61 mouse model, emphasizing this mouse model as a valuable in vivo tool to test new compounds directed against synucleinopathies.