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1 s GRN contribute to disease pathogenesis and neurodegeneration.
2 r toxicity of misfolded proteins and prevent neurodegeneration.
3 PP metabolism with important implications in neurodegeneration.
4 ed in human development, and is disrupted by neurodegeneration.
5 torage disorder characterised by progressive neurodegeneration.
6 the microglial response to tau pathology, or neurodegeneration.
7 eutic approaches for alpha-synuclein induced neurodegeneration.
8 eregulation underlies memory deficits during neurodegeneration.
9 ping new therapies for BBB repair to control neurodegeneration.
10 pathway of tau aggregation and the resulting neurodegeneration.
11 es a mechanistic link between DNA repair and neurodegeneration.
12 y be a suitable therapeutic strategy against neurodegeneration.
13 and conformational Tau changes, and undergo neurodegeneration.
14 isrupted cortical lamination, and widespread neurodegeneration.
15 S cortex and elucidate its relationship with neurodegeneration.
16 ical coherence tomography (SD-OCT) evaluated neurodegeneration.
17 trictions and oxidative stressed neurons and neurodegeneration.
18 es, are unable to induce acute dopamine (DA) neurodegeneration.
19 c hormones considered therapeutic targets in neurodegeneration.
20 eads to synaptic pathology and ultimately to neurodegeneration.
21 al growth factor-A (VEGF-A), contributing to neurodegeneration.
22 they have protective factors for amyloid and neurodegeneration.
23 wledge about the TBK1 functions relevant for neurodegeneration.
24 ed individuals and often is an early sign of neurodegeneration.
25 abnormalities, and no signs of dopaminergic neurodegeneration.
26 eostasis but also constitutes a mechanism of neurodegeneration.
27 cluding tauopathy, synaptic dysfunction, and neurodegeneration.
28 ll loss in a zebrafish model of dopaminergic neurodegeneration.
29 ential feed-forward loop that contributes to neurodegeneration.
30 network formation and function that precede neurodegeneration.
31 fully understood how these mutations lead to neurodegeneration.
32 lipids linked to both neural development and neurodegeneration.
33 propensity for altered systemic immunity and neurodegeneration.
34 rtant role both during brain development and neurodegeneration.
35 ole of somatic mutations in myeloid cells in neurodegeneration.
36 other AD biomarkers, and imaging evidence of neurodegeneration.
37 ing a direct link between neuroblastomas and neurodegeneration.
38 chain (NfL) has been suggested a marker for neurodegeneration.
39 ns that may have a deleterious impact during neurodegeneration.
40 V600E) mutation in the EMP lineage may cause neurodegeneration.
41 ese mice developed epilepsy without signs of neurodegeneration.
42 pha-syn accumulation, neuroinflammation, and neurodegeneration.
43 g pathway promotes neurogenesis and inhibits neurodegeneration.
44 sult more from diffuse immune mechanisms and neurodegeneration.
45 fidelity and ribosome stalling, resulting in neurodegeneration.
46 tracer to non-tau molecules associated with neurodegeneration.
47 e strand breaks and ATM defects and triggers neurodegeneration.
48 a and exerts neuroprotective effects against neurodegeneration.
49 lve with disease progression but precede NMJ neurodegeneration.
50 ncer, diabetes, cardiovascular diseases, and neurodegeneration.
51 evelopment of various pathologies, including neurodegeneration.
52 and (18)FDG-PET parameters related to brain neurodegeneration.
53 prevented neuronal loss in an acute model of neurodegeneration.
54 the EMP lineage in mice can drive late-onset neurodegeneration.
55 rostructural tissue integrity, and secondary neurodegeneration.
56 indirect trauma to the nerve and subsequent neurodegeneration.
57 g a secondary effect of neuroinflammation or neurodegeneration.
58 genous CNS immune mechanisms, can affect CNS neurodegeneration.
59 rlier mortality and age-dependent, selective neurodegeneration.
60 hat the impaired IGF-I system contributes to neurodegeneration.
61 mTORC1 signaling, and impaired autophagy in neurodegeneration.
62 ation of several diseases, such as cancer or neurodegeneration.
63 cortical lamination, and to protect against neurodegeneration.
64 pin) mutants, a Drosophila model of LSD-like neurodegeneration.
65 g is a valid marker of clinical symptoms and neurodegeneration.
66 diseases ranging from infection to cancer to neurodegeneration.
67 basal autophagy, a key mechanism suppressing neurodegeneration.
68 (MS), contributes to axonal dysfunction and neurodegeneration.
69 genes previously associated with cerebellar neurodegeneration.
70 dized cholesterol metabolite associated with neurodegeneration.
71 widely felt to play a key role in promoting neurodegeneration.
72 potential molecular target for treatment of neurodegeneration.
73 of these protein aggregates leads to AD-like neurodegeneration.
74 ion to homeostasis, and their involvement in neurodegeneration.
75 lial numbers and ameliorated mHTTx1-mediated neurodegeneration.
76 trophy is characterized by demyelination and neurodegeneration.
77 n the somatosensory cortex prior to signs of neurodegeneration.
78 re directly linked by distinct mechanisms to neurodegeneration.
79 is paramount for understanding their role in neurodegeneration.
80 its homolog Tau, which has various roles in neurodegeneration.
81 ent, were associated with greater AD-pattern neurodegeneration.
82 ter ATP7A because ATP7A null mutations cause neurodegeneration.
83 brain injury, Parkinson's disease, and other neurodegenerations.
84 n glaucoma and potentially other age-related neurodegenerations.
85 th old mhAPP mice, whereas at later stage of neurodegeneration (6 month) basal synaptic transmission
87 es) is not directly related to the degree of neurodegeneration across various vulnerable neuronal pop
88 rmative cognition, we measured AD-associated neurodegeneration (AD signature cortical thickness; ADSC
89 s, p = 6.8 x 10-6) and in vivo markers of AD neurodegeneration (ADNI, volume loss within the entorhin
93 f neuronal injury signaling that drives both neurodegeneration and axon regeneration, yet little is k
99 sessed by microperimetry is related to brain neurodegeneration and could be a useful biomarker for id
101 ingly recognized as important mechanisms for neurodegeneration and dementia associated with Alzheimer
102 behavioural deficit during amyloid-dependent neurodegeneration and demonstrate that microglial RAGE a
103 dylcholine (LPC), a molecule associated with neurodegeneration and demyelination, elicits NLRP3 and N
104 resembles several aspects of SPMS, including neurodegeneration and disease progression driven by the
108 at the hair cell synapse that later leads to neurodegeneration and exacerbates age-related hearing lo
110 mic stroke lesion volume but also attenuated neurodegeneration and improved poststroke sensorimotor f
111 of the nuclear export adaptor SRSF1 prevents neurodegeneration and locomotor deficits in a Drosophila
112 To identify pathways involved in subsequent neurodegeneration and loss of brain mass in the cKO cort
115 arkin promoted earlier onset of dopaminergic neurodegeneration and motor defects in the PD-mito-PstI
118 ar to anatomical, that may contribute to RGC neurodegeneration and optic atrophy are tackled in an in
119 tanding the molecular pathophysiology of RGC neurodegeneration and optic atrophy, is key to broadly u
120 y help develop urgently needed therapies for neurodegeneration and other age-dependent pathologies.
121 MGRN1 deficiency is closely associated with neurodegeneration and prenatal and neonatal mortality, w
122 st time that the extent of early hippocampal neurodegeneration and progressive microstructural change
123 ar antigen 1 (TIA1) in vivo protects against neurodegeneration and prolongs survival in transgenic P3
124 depletion robustly enhances TDP-43-mediated neurodegeneration and promotes the formation of stress g
126 rkedly upregulated in a mouse model of acute neurodegeneration and reactive gliosis, which was induce
127 atic brain injury is associated with greater neurodegeneration and reduced memory performance in indi
128 llows for both rapid and robust diagnosis of neurodegeneration and segregation between different deme
129 development of neurological signs, prevented neurodegeneration and significantly prolonged survival.
130 l mechanism for the observed tissue specific neurodegeneration and the role of environmental factors
131 AP kinase pathway in microglia as a cause of neurodegeneration and this offers opportunities for ther
132 ndent degenerative disorders such as cancer, neurodegeneration and tissue atrophy, and in accelerated
133 rticularly ceramide and glucosylceramide, to neurodegeneration and to motor unit dismantling in amyot
134 athways linking Abeta to synaptotoxicity and neurodegeneration and to new targets for therapeutic int
136 tochondrial dynamics induced by alpha-syn on neurodegeneration and whether targeting this pathway has
138 human diseases, including diabetes mellitus, neurodegeneration, and cancer, thus opening up the poten
140 by extending lifetime in NPC mice, delaying neurodegeneration, and decreasing visceral and neurologi
142 along with widespread hippocampus and cortex neurodegeneration, and learning and memory defects.
144 ultiple human diseases, including cancer and neurodegeneration, and modulation of non-AUG usage may r
146 tochondrial calcium overload in LRRK2-driven neurodegeneration, and suggest possible interventions th
147 t lack of arginylation in the brain leads to neurodegeneration, and suggests that alpha-syn arginylat
149 ties in neuroimaging measures of amyloid and neurodegeneration are correlated with odor identificatio
154 erlying mechanisms between BBB breakdown and neurodegeneration as a basis for developing new therapie
155 uroimaging biomarker modality used to define neurodegeneration associated with Alzheimer disease.
157 on end products (RAGE) in neuroinflammation, neurodegeneration-associated changes, and cognitive dysf
158 SJ1 overexpression can reduce aggregation of neurodegeneration-associated proteins in vitro and in vi
159 Whereas normoxia-treated KO mice die from neurodegeneration at about 60 d, hypoxia-treated mice ev
163 otal of 469 individuals with MCI had data on neurodegeneration biomarkers; of these patients, 107 wer
164 cognitively normal participants had data on neurodegeneration biomarkers; of these, 52 were Abeta-N+
165 Gain of function of the complex leads to neurodegeneration, but ATXN1-CIC is also essential for s
166 ter volumes are often interpreted to reflect neurodegeneration, but studies investigating the cellula
167 synuclein (alpha-syn) is a central player in neurodegeneration, but the mechanisms triggering its pat
168 images, are commonly interpreted to reflect neurodegeneration, but this assumption has not been test
169 nship between PNS function and AD-associated neurodegeneration by testing two competing hypotheses in
170 s been demonstrated in preclinical models of neurodegeneration by virtue of promoting neuronal surviv
171 implicated in several pathologies, including neurodegeneration, cancer, infection, immunodeficiency,
172 These findings indicate that TDP-43-mediated neurodegeneration causes impaired chromatin dynamics tha
173 ong neural circuits are thought to result in neurodegeneration causing Alzheimer's disease, progressi
174 paminergic neurons in vivo, resulting in the neurodegeneration characteristic of PD.SIGNIFICANCE STAT
175 Loss of proteostasis underlies ageing and neurodegeneration characterized by the accumulation of p
176 ation, with progressive age-related signs of neurodegeneration, characterized by clustering of activa
177 on elevation that is closely associated with neurodegeneration, cognitive loss and parkinsonian featu
179 ell as 9 individuals affected by early-onset neurodegeneration due to genetic disorders of DNA repair
180 pe human alpha-synuclein, which shows robust neurodegeneration, early-onset locomotor deficits, and a
181 thenate kinase 2 gene cause a severe form of neurodegeneration for which no treatment is available.
182 ctivated microglial cells, the first step in neurodegeneration, has been widely demonstrated, and thi
183 ted in playing a unique and critical role in neurodegeneration; however, structural similarities betw
184 f glycogen metabolism in brain functions and neurodegeneration, impairment of the glycogenolytic acti
185 rotective factors for amyloid and AD-pattern neurodegeneration in a population-based sample and to te
186 on of cognitive deficits, neuroinflammation, neurodegeneration in a transgenic mouse model of tauopat
188 llar amyloid deposits, which are linked with neurodegeneration in Alzheimer and Parkinson disease, an
191 Chronic inflammation is one of the causes of neurodegeneration in Amyotrophic lateral sclerosis (ALS)
192 s have proven effective against tau-mediated neurodegeneration in animal models, and because COX- and
199 designed to isolate genes whose loss causes neurodegeneration in Drosophila photoreceptor neurons.
202 tein was not sufficient to protect mice from neurodegeneration in G70S/- mice, showing that the mutan
204 way of thinking about the possible cause of neurodegeneration in HIV-1-seropositive patients, which
205 te a subset of PIs as potential mediators of neurodegeneration in HIV-associated neurocognitive disor
206 ght-activated caspase (Caspase-LOV) to study neurodegeneration in larval and adult Drosophila Using t
208 -2-HG accumulation, leukoencephalopathy, and neurodegeneration in mice, thereby offering new insights
209 ings demonstrate that SSC drives excitotoxic neurodegeneration in MoCD and introduce NMDA-R antagonis
212 retinal layers show atrophy associated with neurodegeneration in multiple sclerosis when measured wi
215 f hypoxia can be used to prevent and reverse neurodegeneration in other animal models, and to determi
216 implicated in substantia nigra dopaminergic neurodegeneration in Parkinson's disease (PD), but how t
217 egative ventral tier, which is vulnerable to neurodegeneration in Parkinson's disease, and the calbin
218 in blood is a potential prognostic marker of neurodegeneration in patients with Huntington's disease.
220 ansion in the deubiquitinase ataxin-3 causes neurodegeneration in Spinocerebellar Ataxia Type 3 (SCA3
224 of LSD1 in adult mice leads to paralysis and neurodegeneration in the hippocampus and cortex and sugg
225 ate at the sites of active demyelination and neurodegeneration in the multiple sclerosis brain and ar
226 ive flexibility." It has been suggested that neurodegeneration in the pathway between the centromedia
228 s Parkinson's disease, presumably by driving neurodegeneration in vulnerable neuronal target populati
231 eceptor required for microglial responses to neurodegeneration, including proliferation, survival, cl
232 genesis, neuroinflammation, and tau-mediated neurodegeneration independently of amyloid-beta patholog
234 leads to hippocampus dysfunction typified by neurodegeneration, inflammation, altered neurogenesis, a
241 A first step toward understanding cochlear neurodegeneration is to identify the cause of initial ex
244 e phosphorylation system (OXPHOS), occurs in neurodegeneration, it is postulated that such defects ar
245 esized to be responsible for synapse damage, neurodegeneration, learning, and memory deficits in AD.
246 ne of evidence to suggest that AD-associated neurodegeneration links to altered PNS regulation during
247 flies results in robust Abeta accumulation, neurodegeneration, locomotor dysfunction, and reduced li
248 ly related to both more severe AD-associated neurodegeneration (lower ADSCT scores) and worse cogniti
251 e absence of peroxisomes, reduced viability, neurodegeneration, mitochondrial abnormalities, and accu
254 mulation including tau hyperphosphorylation, neurodegeneration, neuroinflammation and microhemorrhage
256 PS cDKO mice display classical features of neurodegeneration occurring in Alzheimer's disease inclu
257 lta14 ALS mouse-antibody system we show that neurodegeneration occurs in the absence of FUS protein a
260 egenerative disorders defined by progressive neurodegeneration of the corticospinal tract motor neuro
263 included with those of beta-amyloidosis and neurodegeneration or neuronal injury to more fully chara
264 ng tau PET, and normal (N-) or abnormal (N+) neurodegeneration or neuronal injury using cortical thic
265 TEMENT This study provides new insights in a neurodegeneration pathway triggered by the absence of sp
266 LSD1 induces transcription changes in common neurodegeneration pathways, along with the re-activation
268 er prevalence may account for differences in neurodegeneration patterns between Abeta-N+ and Abeta+N+
269 taucipir binding corresponds to the expected neurodegeneration patterns in nonamnestic AD, with poten
270 ween patients with distinct SNAP (Abeta- and neurodegeneration-positive [Abeta-N+]) subtypes and thei
271 Neuroinflammation is an integral part of the neurodegeneration process inherent to several aging dysf
272 cells (RGCs), are particularly vulnerable to neurodegeneration related to mitochondrial dysfunction.
276 Lipopolysaccharide-induced in vitro enteric neurodegeneration requires the presence of palmitate and
278 ) mutants display many phenotypes, including neurodegeneration, segmentation, patterning and planar p
279 ic activity that leads to excitotoxicity and neurodegeneration.SIGNIFICANCE STATEMENT Dendritic spine
280 ar to be good predictors of vulnerability to neurodegeneration.SIGNIFICANCE STATEMENT The inadequate
281 d retrograde JNK signaling and protects from neurodegeneration, suggesting that these kinases may rep
282 MC(+) participants had significantly greater neurodegeneration than CMC(-) participants but did not d
283 e revealed lessons about inflammation-driven neurodegeneration that can be applied to other neurodege
284 ase is Leigh syndrome, an episodic, subacute neurodegeneration that can lead to death within the firs
285 gain unique perspectives into mechanisms of neurodegeneration that contribute to ALS pathogenesis.
286 s disease (HD) is characterized by selective neurodegeneration that preferentially occurs in the stri
287 ensitive to iron accumulation, one marker of neurodegeneration, that (i) secondary thalamic alteratio
288 s) have identified hundreds of risk loci for neurodegeneration, the mechanisms by which these loci in
289 mary events and sufficiently contributory to neurodegeneration to be useful targets for therapy of se
290 key roles in multiple diseases ranging from neurodegeneration to diabetes and metastatic cancer.
291 onths, the hippocampal neuroinflammation and neurodegeneration typically observed in unlesioned P301S
292 that the (G4C2)n repeat causes toxicity and neurodegeneration via a gain-of-toxic function mechanism
295 enetic understanding of lysosomal defects in neurodegeneration, we explore why some of these orphan d
297 -fat diet (HFD) is associated with myenteric neurodegeneration, which in turn is associated with dela
298 microglia-type has the potential to restrict neurodegeneration, which may have important implications
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