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1 is associated with neuronal dysfunction and neurodegeneration.
2 s is a central part of innate immune-induced neurodegeneration.
3 ological disorders and is thought to precede neurodegeneration.
4 further implicate the importance of glia in neurodegeneration.
5 ntial option to ameliorate alpha-syn-induced neurodegeneration.
6 ly dynamic functions in neurodevelopment and neurodegeneration.
7 or of complex, multicomponent condensates in neurodegeneration.
8 s the vicious cycle between inflammation and neurodegeneration.
9 al autophagy develop early onset progressive neurodegeneration.
10 ain Receptors (DDRs) is poorly understood in neurodegeneration.
11 ed both aberrant Purkinje neuron spiking and neurodegeneration.
12 ronmental exposure has also been linked with neurodegeneration.
13 tem and implicate RQC dysfunction in causing neurodegeneration.
14 ain iron homeostasis is the primary cause of neurodegeneration.
15 d progressive motor decline and dopaminergic neurodegeneration.
16 n antioxidant suppressed the p.N237S-induced neurodegeneration.
17 ective mitochondrial turnover contributes to neurodegeneration.
18 on of lysosome-like organelles that precedes neurodegeneration.
19 acute tissue damage, infection, cancer, and neurodegeneration.
20 on of abnormal tau aggregates and subsequent neurodegeneration.
21 results in frataxin deficiency and eventual neurodegeneration.
22 tood, particularly at early stages preceding neurodegeneration.
23 is causally involved in basic principles of neurodegeneration.
24 w kinetics of neuronal mitophagy, leading to neurodegeneration.
25 of the changes undergone in the brain during neurodegeneration.
26 in in the CSF was assessed as a biomarker of neurodegeneration.
27 a stage prior to widespread synapse loss and neurodegeneration.
28 Fas neuroimmune signaling in AUD hippocampal neurodegeneration.
29 NS where these cells cause demyelination and neurodegeneration.
30 pathophysiological processes associated with neurodegeneration.
31 lia-like cells, which are central players in neurodegeneration.
32 nthase kinase 3beta (GSK3beta) implicated in neurodegeneration.
33 n of neurofilament measures as biomarkers of neurodegeneration.
34 e protein are relevant pathogenic species in neurodegeneration.
35 cts the degree of progressive post-traumatic neurodegeneration.
36 ial-associated neuroinflammation and chronic neurodegeneration.
37 optosis and cerebral pathology in stroke and neurodegeneration.
38 tion of HSF1 target genes in both cancer and neurodegeneration.
39 ns in NHE6 cause complex, slowly progressive neurodegeneration.
40 normal locomotion and prevents age-dependent neurodegeneration.
41 matory activity and reduction of the risk of neurodegeneration.
42 ar pathways through which TDP-43 may mediate neurodegeneration.
43 general and convergent mechanism leading to neurodegeneration.
44 ell autonomous contribution of astrocytes to neurodegeneration.
45 n active lesions amplifies demyelination and neurodegeneration.
46 eterious cascade involving tau pathology and neurodegeneration.
47 ns were stained with Fluoro-Jade C to assess neurodegeneration.
48 gents that counter proteotoxicity underlying neurodegeneration.
49 on of the virus through axons and subsequent neurodegeneration.
50 entially interesting approach for studies on neurodegeneration.
51 underscoring their therapeutic potential in neurodegeneration.
52 s9 inhibition of genes that are critical for neurodegeneration.
53 gical disorders associated with dopaminergic neurodegeneration.
54 ells promotes capillary ischemia and retinal neurodegeneration.
55 odel of AD exacerbated amyloid-beta42-driven neurodegeneration.
56 torsinA LOF-mediated abnormal movements and neurodegeneration.
57 n and assembly with therapeutic potential in neurodegeneration.
58 armful to neurons in vivo in mice with prion neurodegeneration.
59 zheimer's disease-causing Psen1 mutations on neurodegeneration.
60 5hmC epigenetics in the events leading to AD neurodegeneration.
61 hat causes it, and whether it contributes to neurodegeneration.
62 the cognitive prognosis during Abetao-driven neurodegeneration.
63 rable due to, for example, aging and ongoing neurodegeneration.
64 comorbid pathologies associated with greater neurodegeneration.
65 bnormalities in survival, motor function, or neurodegeneration.
66 , a neuroinflammatory "globoid" reaction and neurodegeneration.
67 s, insulin dysregulation could contribute to neurodegeneration.
68 antial genetic component and immune-mediated neurodegeneration.
69 , resulted in worsened disease and increased neurodegeneration.
70 s that occur between brain cell types during neurodegeneration.
71 for conditions of cognitive deficit such as neurodegeneration.
72 ounter functional decline in brain aging and neurodegeneration.
73 ecal space of brains affected by age-related neurodegeneration.
74 ronal mitochondria, decreases with aging and neurodegeneration.
75 ntribute to age-related and genetic forms of neurodegeneration.
76 from glucose to lipid is a key mechanism in neurodegeneration.
77 ia sequestration contributes to tau-mediated neurodegeneration.
78 al dysfunction, enhanced neuronal death, and neurodegeneration.
79 ommon feature of severe mental illnesses and neurodegeneration.
80 ive T(2) MRI could be used as a biomarker of neurodegeneration.
81 dust with respect to their potential role in neurodegeneration.
82 ses, including cancer, diabetes, obesity and neurodegeneration.
83 t compete with destructive processes driving neurodegeneration.
84 g the events that convert normal ageing into neurodegeneration.
85 ar senescence as a cause or a consequence of neurodegeneration.
86 onnecting glycosyltransferase dysfunction to neurodegeneration.
87 re recruited from the Sant Pau Initiative on Neurodegeneration.
88 SCA3) belongs to the family of polyglutamine neurodegenerations.
93 ET data of 35 patients with amyloid-positive neurodegeneration, 19 patients with amyloid-negative neu
95 thogenesis, but longitudinal Abeta, tau, and neurodegeneration (A/T/N) measurements in the same indiv
96 vated the inflammatory response in aging and neurodegeneration, a process modulated by melatonin.
97 w it relates to amyloid and tau pathology or neurodegeneration across the Alzheimer's disease continu
98 ventral route is damaged, as in the case of neurodegeneration affecting the anterior temporal lobe,
99 ion exacerbates the development of secondary neurodegeneration after stroke beyond its acute effects
104 and demonstrate that neuronal PTP1B hastens neurodegeneration and cognitive decline in this model of
105 rine TBI, is associated with arrested axonal neurodegeneration and cognitive recovery, benefits that
106 al predictors of longitudinal post-traumatic neurodegeneration and compared the variance in brain atr
107 formed, is sufficient to significantly delay neurodegeneration and counteract tau-induced expression
108 yndrome, a human disorder characterized with neurodegeneration and cytochrome c oxidase deficiency.
111 nia, respiratory insufficiency, and variable neurodegeneration and diffusion restriction in cerebral
112 CNS in the context of neuroinflammation and neurodegeneration and discuss how these interactions sha
114 se for the tracking of early stage events in neurodegeneration and for investigating actin's interact
116 g drug target for a wide disease range, from neurodegeneration and infections to cancer and cardiovas
118 phorylation is an early step in tau-mediated neurodegeneration and is associated with intracellular a
119 rt the idea that the retina reproduces brain neurodegeneration and is highly involved in PD pathology
120 red mechanism-synaptopathy-between Alzheimer neurodegeneration and its best-established epigenetic ri
121 rand breaks (DSBs); lesions that can trigger neurodegeneration and neurodevelopmental dysfunction, re
122 inistration of PAP-1 significantly inhibited neurodegeneration and neuroinflammation in multiple anim
126 tion provides a powerful system for studying neurodegeneration and plasticity across prolonged develo
127 elta/Delta) mice was extended due to delayed neurodegeneration and resistance to death upon fasting.
128 abolism due to GARP mutations contributes to neurodegeneration and suggest that inhibiting sphingolip
129 athogenesis and treatment of NIHL as well as neurodegeneration and synaptic damage in the brain.
130 sufficient to highly exacerbate tau-mediated neurodegeneration and tau-induced gene expression change
131 inning near the onset of nigral and cortical neurodegeneration and the robust PD-like motor syndrome
132 asured parafoveal GCIPL thickness to monitor neurodegeneration and to predict the risk of cognitive w
133 eneration, 19 patients with amyloid-negative neurodegeneration, and 17 healthy controls were included
134 an diseases such as cancer, asthma, allergy, neurodegeneration, and autoimmune diseases they have gai
138 e moment has been on non-specific markers of neurodegeneration, and in particular, multiple studies o
140 o the pathways linking tau, amyloid-beta and neurodegeneration, and may facilitate clinical trials of
142 ameliorates inflammation, vascular leakage, neurodegeneration, and neovascularization associated wit
143 ew focuses on cGAS-STING signaling in aging, neurodegeneration, and neuroinflammation, and on therape
144 eletal and cardiac myopathies, diabetes, and neurodegeneration, and partly results from increased Ca(
145 stations of tau pathobiology, independent of neurodegeneration, and provide a mechanism for the neuro
146 iated with human diseases such as cancer and neurodegeneration, and so an in-depth understanding of h
147 tive decline, pathological tau accumulation, neurodegeneration, and transition to a diagnosis of MCI/
148 cal mechanisms through which TDP-43 mediates neurodegeneration appears complex, and unravelling these
150 petitive mild traumatic brain injury-induced neurodegeneration are unknown and antemortem diagnostic
152 ions may explain how stereotyped patterns of neurodegeneration arise in humans or define a not yet id
154 et for its involvement in the first steps of neurodegeneration as well as in cancer onset and progres
155 s, African American participants had greater neurodegeneration, as measured by decreased cortical vol
156 uce chronic neuroinflammation and associated neurodegeneration, as well as related motor and cognitiv
157 kinase that phosphorylates hnRNPA2, reduces neurodegeneration associated with chimeric hnRNPA2 D290V
158 aphy study to longitudinally compare retinal neurodegeneration between 52 patients on continuous 4-AP
159 ied by using the A (amyloid beta)/T (tau)/N (neurodegeneration) biomarker classification system.
160 xisting link between Golgi fragmentation and neurodegeneration but also demonstrate that pathogenic v
161 loss is not due to generalized, progressive neurodegeneration, but may be mediated by specific effec
162 eacetylase capable of countering age-related neurodegeneration, but the basis of Sirt1 neuroprotectio
163 , rare variation in TET2 may confer risk for neurodegeneration by altering the homeostasis of key agi
165 the histone demethylase LSD1 in tau-induced neurodegeneration by showing that LSD1 localizes to path
166 f phagocytic glia as double-edged players in neurodegeneration-by clearing neurotoxic protein aggrega
170 at RNA binding-deficient TDP-43 (produced by neurodegeneration-causing mutations or posttranslational
171 Aggregation of tau has been implicated in neurodegeneration, cellular toxicity and the propagation
172 is the main risk factor for dementia-related neurodegeneration, changes in the timing or nature of th
173 eral nervous systems was normalized, and the neurodegeneration, chronic neuroinflammation and loss of
174 ological age in health and disease including neurodegeneration, dementia and other brain phenotypes.
175 abolic stress, which could explain why local neurodegeneration does not remain confined, but eventual
177 cal inflammatory activity is associated with neurodegeneration early in MS which reinforces the use o
178 avioural changes can represent a prodrome to neurodegeneration; empirical data are required to explor
180 tau phosphorylation, amyloid pathology, and neurodegeneration, especially when protective calcium bi
182 ine, in the context of the amyloid, tau, and neurodegeneration framework, the available evidence and
184 proteins, with causative roles in neoplasia, neurodegeneration, hepatosteatosis, and other pathologie
185 ry amino acids are important determinants of neurodegeneration in a Drosophila model of LRRK2 PD.
186 function yet a rise in sensitive measures of neurodegeneration in a preHD cohort approximately 24 yea
188 endogenous immune signaling axis that drives neurodegeneration in AD and has strong implications for
194 ocephaly with early onset seizures (MCSZ) to neurodegeneration in ataxia oculomotor apraxia-4 (AOA4)
195 ion alone causes mitochondrial pathology and neurodegeneration in both flies and human neurons, impli
196 tic product pyruvate strongly protected from neurodegeneration in both rat and mouse models of glauco
197 egradation, the precise mechanism leading to neurodegeneration in both sporadic and familial PD upon
200 quitously expressed polyQ proteins can cause neurodegeneration in distinct brain regions in different
201 n synthesis and blocks LRRK2 G2019S-mediated neurodegeneration in Drosophila and rat primary neurons.
203 ty to RBPs, such as hnRNP A1, play a role in neurodegeneration in EAE with important implications for
205 r produces toxic proteins that contribute to neurodegeneration in fragile X-associated tremor/ataxia
212 ment and whether these effects contribute to neurodegeneration in Niemann-Pick disease type C (NPC).
216 and ONL measures may be novel biomarkers of neurodegeneration in PMS that appear to be unaffected by
217 hin glycosyltransferases are associated with neurodegeneration in recognition of the fact that these
224 disease (AD) is characterized by progressive neurodegeneration in the cerebral cortex, histopathologi
225 omise of plasma NfL as a biomarker of active neurodegeneration in the detection and tracking of Alzhe
226 (NLGN1) is affected early in the process of neurodegeneration in the hippocampus, and specifically b
229 expression of tau affects alpha-syn-induced neurodegeneration in vivo, we generated triple transgeni
232 and female mice was sufficient to rescue the neurodegeneration, increase survival time, and improve c
236 Here, we show that LRRK2 G2019S-induced neurodegeneration is critically dependent on dietary ami
238 nduced glutamatergic neurodegeneration; this neurodegeneration is rescued by loss of tdp-1, suggestin
244 ging biomarkers of amyloid (A), tau (T), and neurodegeneration (N) for potential racial differences a
245 ive information on amyloid (A), tau (T), and neurodegeneration (N) status as required by recent bioma
247 of NT1 for AD versus a nonspecific marker of neurodegeneration (neurofilament light [NfL]) were also
248 span of treated animals, rescued the lethal neurodegeneration, normalized the locomotor behavioural
249 no acid diet of the range tested, PD-related neurodegeneration occurs in an age-related manner, but i
252 ween amyloid-positive and -negative forms of neurodegeneration on the basis of different (18)F-florta
253 autophagy are critical determinants of LRRK2 neurodegeneration, opening up possibilities for future t
255 using various imaging modalities may reflect neurodegeneration or other AD-related pathology on a cel
256 nterventions for diseases like brain cancer, neurodegeneration, or age-associated inflammatory proces
258 ed on the native DNA i-motifs (iMs) found in neurodegeneration- or carcinogenesis-related genes.
260 it age-dependent neurofibrillary tangles and neurodegeneration, overexpressed CX3CL1 in both male and
262 eases such as pantothenate kinase-associated neurodegeneration (PKAN) and result in low levels of coe
263 with multiple in vitro targets underpinning neurodegeneration points to the potential interest of th
264 established by structural damage, e.g. from neurodegeneration possibly as result from genetic variab
265 sed by stroke (post-stroke aphasia, PSA) and neurodegeneration (primary progressive aphasia, PPA) hav
267 dly and drives a potent pro-inflammatory and neurodegeneration-related gene program, evidenced by inc
271 lusion: PES of (18)F-FDG-ADCRP, a measure of neurodegeneration, shows close correspondence with the e
272 hondria dysfunction and neuroinflammation in neurodegeneration.SIGNIFICANCE STATEMENT Our study sugge
274 leads to codon-specific ribosome pausing and neurodegeneration, suggesting that these non-redundant G
275 es, but no association to protein markers of neurodegeneration, suggesting that vCSF-cfmtDNA release
276 tion of mTOR robustly prevented glaucomatous neurodegeneration, supporting a damaging role for IOP-in
277 ding biomarkers for Abeta and tau pathology, neurodegeneration, synaptic dysfunction, and inflammatio
278 F-cfmtDNA levels to known protein markers of neurodegeneration, synaptic vesicles and mitochondrial i
279 nk between axonal injury and the progressive neurodegeneration that is commonly seen after moderate/s
280 ade resulting in synaptodendritic damage and neurodegeneration that lead to cognitive impairment.
281 eals a degree of progressive instability and neurodegeneration that was not apparent during the typic
282 with data from patients with non-TDP-related neurodegenerations, they demonstrate a direct relationsh
283 gans results in stress-induced glutamatergic neurodegeneration; this neurodegeneration is rescued by
284 il formation, is one of the major drivers of neurodegeneration through disruption of cellular functio
285 degeneration, and potentially other forms of neurodegeneration, through a pathway dependent upon micr
288 energy metabolism precipitates a pattern of neurodegeneration via cell death across disparate but li
289 isomal acyl-CoA oxidase 1 (ACOX1) gene cause neurodegeneration via distinct molecular pathways in gli
293 r vulnerability to dysfunction, atrophy, and neurodegeneration when regulation is lost due to genetic
294 y distinct neuroimaging patterns of regional neurodegeneration, which are paralleled by heterogeneous
295 iron deposition and both tau aggregation and neurodegeneration, which help advance our understanding
296 termed decrepit) that results in adult-onset neurodegeneration with a stereotypical neuroanatomical p
297 nockout (KO) rats exhibit progressive nigral neurodegeneration with about 50% dopaminergic cell loss
298 iffuse axonal injury triggers post-traumatic neurodegeneration, with axonal damage leading to Walleri
299 viding insights into molecular mechanisms of neurodegeneration, with wide application to human diseas
300 complex interplay between Abeta, aging, and neurodegeneration within the most vulnerable neurons in