ライフサイエンスコーパス: memory loss

1 ribute to long-term cognitive impairment and memory loss.

2 Abeta, likely reflecting normal, age-related memory loss.

3 de as senile plaques, neurodegeneration, and memory loss.

4 ressive neurodegenerative disease leading to memory loss.

5 nsulin signaling, synapse deterioration, and memory loss.

6 luded depression, explosivity and short-term memory loss.

7 e design of improved clinical treatments for memory loss.

8 plaques, progressive neurodegeneration, and memory loss.

9 which is potentially linked to age-dependent memory loss.

10 aptic breakdown, cell death, and devastating memory loss.

11 cation, often before the appearance of overt memory loss.

12 FMS and 43 control subjects) presenting with memory loss.

13 is recurrent, transient episodes of isolated memory loss.

14 elated the levels of these tau proteins with memory loss.

15 ue in diseases and conditions that result in memory loss.

16 at might point to the mechanisms behind such memory loss.

17 fluence its ability to reduce age-associated memory loss.

18 (AD) characteristically presents with early memory loss.

19 lderly patients who present with symptoms of memory loss.

20 ng apart neural mechanisms underlying remote memory loss.

21 sease; the initial phase is characterized by memory loss.

22 olimus had no effect on seizure frequency or memory loss.

23 dementia characterized by mental slowing and memory loss.

24 pathway is defective in age-related spatial memory loss.

25 d psychological effects in humans, including memory loss.

26 ession to dementia in patients with isolated memory loss.

27 s provided clearcut evidence of time-related memory loss.

28 sequilibrium, neck stiffness, dysphagia, and memory loss.

29 sented with double vision, unsteady gait and memory loss.

30 neurodegenerative disorder characterized by memory loss.

31 lation of CXCR3 also prevented TDP-43-linked memory loss.

32 o against age-related cognitive function and memory loss.

33 novative therapeutic approaches for treating memory loss.

34 with a burden of side effects, most notably memory loss.

35 icient to impede AD-associated pathology and memory loss.

36 of LGI1 and its relationship to seizures and memory loss.

37 millions patients with cognitive decline and memory loss.

38 ar gene-dose-dependent prevention of spatial memory loss.

39 -two of the three most important targets for memory loss.

40 symptoms including depression, anxiety, and memory loss.

41 l conditions such as depression, anxiety and memory loss.

42 where olfactory deficits precede detectable memory loss.

43 but this dysfunction was not associated with memory loss.

44 rtex, as a substrate of age-related episodic-memory loss.

45 its will allow future targeted treatment for memory loss.

46 release, failure of synaptic plasticity, and memory loss.

47 can be further explored in a mouse model of memory loss.

48 oid production, tau hyperphosphorylation and memory loss.

49 pression in either MBn or DAn impairs normal memory loss.

50 er's disease (AD) and related tauopathies is memory loss.

51 the brain leads to differential patterns of memory loss.

52 ndependently of Abeta, eventually leading to memory loss.

53 erative disorder that may cause irreversible memory loss.

54 C, was sufficient to produce METH-associated memory loss.

55 , and LTP dysfunction is thought to underlie memory loss.

56 polymerization contributes to age-associated memory loss.

57 ign of preclinical AD and may predict future memory loss.

58 astrocytic A2A receptor levels contribute to memory loss.

59 in aged flies protected against APP-induced memory loss.

60 s of Alzheimer's disease (AD) and consequent memory loss.

61 ermines the pattern and extent of retrograde memory loss?

62 ities (1.6 [1.5-1.8]), pain (1.6 [1.5-1.7]), memory loss (1.8 [1.6-2.0]), dizziness (1.7 [1.6-1.8]),

63 disorders (27%), speech disorders (20%), and memory loss (19%).

64 tic movements (4), psychiatric features (3), memory loss (2), and insomnia (2).

65 4% vs. 6.3%), muscle pain (23.1% vs. 10.1%), memory loss (29.2% vs. 4.8%), and joint pain (47.5% vs.

66 .7%]), pain (129 [35.8%] vs 92 [29.9%]), and memory loss (72 [20.0%] vs 49 [15.9%]) were the most pre

67 se sensitivity (12.0 vs 3.0 days, P = .004), memory loss (9.0 vs 4.0 days, P = .04), nausea (9.0 vs 3

68 ys or weeks and (ii) remote autobiographical memory loss: a loss of memories for salient, personally

69 cally solvable quantum model describing this memory loss across an integrability-chaos transition und

70 st the existence of a conserved mechanism of memory loss across the AD models, this mechanism being m

71 Memory loss after brain injury can be a source of consid

72 se series of patients with acute psychogenic memory loss (also known as dissociative/functional amnes

73 amates using a model of amyloid beta induced memory loss and a transgenic mouse model of Alzheimer's

74 interpretation of these results, namely that memory loss and Abeta(insol) were closely connected, was

75 enilin function in adult mouse brains causes memory loss and age-related neurodegeneration.

76 tion or short durations of INO prevents this memory loss and also attenuates the inflammatory respons

77 th impaired cognitive function, particularly memory loss and Alzheimer disease (AD).

78 , which were correlated with the reversal of memory loss and anxiety-like behavior observed in APP/PS

79 The diagnosis of dementia requires both memory loss and at least one other type of cognitive imp

80 coupling hierarchy deteriorates, predicting memory loss and brain atrophy.

81 neurodegenerative disorder that begins with memory loss and can lead to death.

82 Because significant memory loss and cognitive decline are associated with ne

83 It is marked by severe memory loss and cognitive decline, and currently has lim

84 n cause of dementia, and is characterized by memory loss and cognitive decline, as well as amyloid be

85 ing "tangles" that contribute to accelerated memory loss and cognitive decline.

86 Progressive memory loss and cognitive dysfunction are the hallmark c

87 egenerative disorder characterized by severe memory loss and cognitive impairment.

88 ive neurodegenerative disorder manifested by memory loss and cognitive impairment.

89 ive impairment, a condition that can lead to memory loss and dementia over time.

90 ission in this pathway may be related to the memory loss and dementia that accompanies normal aging a

91 ase), our data might also shed some light on memory loss and dementia.

92 24%-59%), cognitive issues (45%-48%) such as memory loss and difficulty concentrating, and menstrual

93 81 on tau, identified in AD brains, promotes memory loss and disrupts synaptic plasticity by reducing

94 d important factor that leads to accelerated memory loss and eventual dementia.

95 gnaling pathways but accelerates the rate of memory loss and exacerbates mitochondrial dysfunction in

96 0.78, 2.2], and a symptom cluster including memory loss and finger tremor (OR 14, 95% CI: 3.5, 57).

97 before it has progressed to produce evident memory loss and functional decline.

98 a 5-year history of predominantly short-term memory loss and functional impairment.

99 However, some situations such as memory loss and hypertension may require other strategie

100 neurodegenerative disorder characterised by memory loss and impaired cognitive function.

101 odegenerative disease associated with severe memory loss and impaired cognitive skills.

102 the activation of Wnt signaling also rescues memory loss and improves synaptic dysfunction in APP/PS1

103 tion in astrocytic TDP-43 caused progressive memory loss and localized changes in antiviral gene expr

104 tivation, amyloid deposition, demyelination, memory loss and motor and anxiety-like behavioral dysfun

105 echanism by which presenilin mutations cause memory loss and neurodegeneration remains unclear.

106 in the adult mouse brain causes progressive memory loss and neurodegeneration resembling AD, whereas

107 d that NFT formation can be dissociated from memory loss and neurodegeneration.

108 neration in Ts65Dn mice leads to exaggerated memory loss and neuronal degeneration.

109 tellectual dysfunction began with subjective memory loss and objective visuospatial dysfunction and w

110 years with gradual onset and progression of memory loss and personality change.

111 neurodegenerative disorder characterized by memory loss and progressive cognitive impairments.

112 a range of behavioral alterations, including memory loss and psychiatric symptoms.

113 esponsive disorder with prominent short-term memory loss and seizures.

114 BDL animals exhibited short-term memory loss and showed reduced astrocyte coverage of the

115 a and associated behavioral symptoms such as memory loss and sleep disturbance are debilitating.

116 rinic signaling using M1 mAChR PAMs restored memory loss and slowed the progression of mouse prion di

117 changes, irritability, depression, seizures, memory loss and sometimes dementia.

118 , 10 subjects developed symptoms of episodic memory loss and subsequently progressed to fulfil criter

119 gests that ginkgo is of questionable use for memory loss and tinnitus but has some effect on dementia

120 pressive symptoms contributed to accelerated memory loss and vice versa, suggesting that psychologica

121 pocampal dysfunction (i.e. severe short-term memory loss) and three with extensive limbic dysfunction

122 sequelae such as fatigue, weakness, myalgia, memory loss, and depression.

123 generation, synapse loss, neuroinflammation, memory loss, and eventual neurodegeneration.

124 ss is known to induce cognitive impairments, memory loss, and neurodegeneration owing to its potent D

125 prevented dendritic network disorganization, memory loss, and neurodegeneration.

126 ity disorders, as well as suicidal behavior, memory loss, and urinary syndromes; they were inversely

127 gnitive syndrome including seizures, ataxia, memory loss, and/or tremors.

128 ninfected individuals, had increased odds of memory loss (aOR, 2.99; 95% CI, 1.30-7.87) and movement

129 odds ratio [aOR], 9.69; 95% CI, 6.59-14.90), memory loss (aOR, 3.19; 95% CI, 1.36-8.69), movement dis

130 cant symptoms of dementia such as short-term memory loss are already present.

131 d blood brain barrier (BBB) permeability and memory loss are associated with diminution of tight junc

132 Cognitive dysfunction and memory loss are common features of Alzheimer's disease (

133 t that early-stage biomarkers that instigate memory loss are composed of Abeta oligomers.

134 NIFICANCE STATEMENT Cognitive impairment and memory loss are critical public health challenges.

135 Concerns about age-related memory loss are greater in persons who have the apolipop

136 ase, alleviates the synaptic dysfunction and memory loss associated with a mouse model of AD.

137 The mechanisms underlying memory loss associated with Alzheimer's disease and rela

138 als in the hippocampus may contribute to the memory loss associated with Alzheimer's disease.

139 ociated with normal aging to the devastating memory losses associated with Alzheimer disease.

140 These animals showed very early memory loss at 11 weeks old.

141 ation, promoted Abeta clearance, and rescued memory loss at a safe level.

142 e tau multimers correlated consistently with memory loss at various ages in the rTg4510 mouse model.

143 itigate early-life adversity-induced spatial memory losses at 4 and 8 months, it restored hippocampus

144 sleep deprivation does not necessarily cause memory loss but instead leads to the suboptimal storage

145 The natural history of patients with severe memory loss but no other type of cognitive impairment is

146 rong relationship between greater stress and memory loss, but few studies have examined this relation

147 our inquiry into the molecular basis of this memory loss by studying Abeta42-induced enhancement of l

148 Here we show that memory loss can be fully reversed in Tg2576 mice using i

149 following demonstration that Abeta42-induced memory loss can be rescued through genetic silencing or

150 Memory loss characterizes several neurodegenerative diso

151 ent reports provided substantial evidence of memory loss, cognitive decline, and dementia related to

152 Alzheimer's disease (AD) is characterized by memory loss, cognitive decline, and devastating neurodeg

153 subsequent development of disorders such as memory loss, cognitive decline, seizures, and epilepsy.

154 and female CC019 mice displayed significant memory loss compared to controls while no significant ch

155 severity and 2) controls with no subjective memory loss complaints and a score >30 in the Phototest

156 tients presented with 1-52 week histories of memory loss, confusion and seizures.

157 and consequently clinical symptoms, such as memory loss, confusion, and impaired cognitive function.

158 The degree of perceived memory loss correlates with subsequent global cerebral m

159 cade in both AD- and Down's syndrome-related memory loss could be triggered by alterations in APP pro

160 Alzheimer's disease (AD) exhibit progressive memory loss, depression, and anxiety, accompanied by imp

161 disciplinary article compares the pattern of memory loss described in Gabriel Garcia Marquez's One Hu

162 w-up, 48% (n = 10) of patients with isolated memory loss-developed dementia compared with 18% (n = 36

163 The pattern of autobiographical memory loss differed between the psychogenic groups: fug

164 may be associated with fatigue, weight gain, memory loss, difficulty concentrating, cardiovascular di

165 en vestibular vertigo, cognitive impairment (memory loss, difficulty concentrating, confusion) and ps

166 ataxia of gait, in the hemizygote group; and memory loss, dizziness, ataxia, hemiparesis, loss of con

167 rative disorder characterized by progressive memory loss due to aberrant accumulation of misfolded pr

168 umbers of BIS-depressed readings and percent memory loss during sedation, while reducing total diazep

169 results provide a candidate explanation for memory losses during normal aging and indicate that, wit

170 In spite of this memory loss, early experiences influence adult behavior,

171 However, ZIP induces memory loss even in the absence of PKMzeta, and its mech

172 Other documented symptoms were short-term memory loss, executive function deficits, cognitive decl

173 ional documented symptoms include short-term memory loss, executive functional deficits, cognitive de

174 We found that our patients with psychogenic memory loss fell into four distinct groups, which we cat

175 type of dementia, typically characterized by memory loss followed by progressive cognitive decline an

176 anterograde amnesia and extensive retrograde memory loss for both facts and events.

177 age, sex, education level, and self reported memory loss, for the development of depression were 6.5

178 Of the 11 cases of long-term visual memory loss found in the literature, all had amnesia ext

179 ich often entails cognitive disturbances and memory loss, has become a major complication for lupus p

180 Patients with severe isolated memory loss have an increased risk of developing dementi

181 n is used to treat individuals with episodic memory loss; however, studies to date report both enhanc

182 o reduce and/or inhibit two major targets of memory loss i.e. AB 1-42 fibrils and tau paired helical/

183 0-101 years]; P = .29), presenting symptoms (memory loss in 7 of 7 mutation carriers [100%] vs 958 of

184 mory retention in normal animals and reduced memory loss in a murine model of Alzheimer's disease.

185 for transcriptional changes underlying early memory loss in AD by examining pathological, behavioral,

186 d binding, prevents pathological changes and memory loss in AD mouse models and ageing wild-type mice

187 receptor (M1-receptor) can not only restore memory loss in AD patients but in preclinical animal mod

188 Abeta assemblies contribute significantly to memory loss in AD, then successfully targeting them migh

189 limited efficacy of memantine in preventing memory loss in AD.

190 ition may prove useful in the alleviation of memory loss in AD.

191 that targeting brain transcriptome reverses memory loss in AD.

192 rain atrophy is a key factor behind episodic memory loss in aging, but the nature and ubiquity of thi

193 o synapses and may play an important role in memory loss in Alzheimer disease.

194 that the amyloid beta-protein contributes to memory loss in Alzheimer disease.

195 representing a key mechanism that underlies memory loss in Alzheimer's disease (AD) and related tauo

196 The memory loss in Alzheimer's disease (AD) has been linked

197 Memory loss in Alzheimer's disease (AD) is attributed to

198 Consequently, research into the causes of memory loss in Alzheimer's disease continues to centre o

199 6-a potential candidate for the treatment of memory loss in Alzheimer's disease.

200 ance of tau oligomeric forms associated with memory loss in animal models of tauopathy.

201 This suggests that the memory loss in APP+PS1 transgenic mice may model the ear

202 beta42 stimulates PI3K, which in turn causes memory loss in association with an increase in accumulat

203 ated with memory consolidation are linked to memory loss in both circumstances.

204 social deficits, affective disturbance, and memory loss in brain disorders, including autism, schizo

205 However, the reasons for the severe memory loss in diencephalic amnesia remain unknown.

206 lication of this paradigm of Abeta42-induced memory loss in Drosophila to investigate the protective

207 upregulation may contribute to age-dependent memory loss in DS and AD and points to correcting calcin

208 Synapse deterioration underlying severe memory loss in early Alzheimer's disease (AD) is thought

209 The basis for memory loss in early Alzheimer's disease (AD) seems like

210 Memory loss in humans begins early in adult life and pro

211 ed with estrogen depletion, including verbal memory loss in humans, may therefore stem from compromis

212 een established in deterministic models, and memory loss in learning has been seen to act similarly t

213 esia is possibly the most ubiquitous form of memory loss in mammals.

214 progression of AD-like neurodegeneration and memory loss in mice.

215 ignificant correlate of clinical severity of memory loss in mild cognitive impairment (P < .001).

216 rebral blood flow and exacerbates short-term memory loss in multiple mouse models of Alzheimer's dise

217 potential mechanisms for therapies to combat memory loss in normal cognitive aging and dementia.

218 logic changes and prevents brain atrophy and memory loss in p25-transgenic mice.

219 H-blocking agent for the early prevention of memory loss in post-menopausal women.

220 n hippocampus that are linked to age-related memory loss in rats.

221 er, and significantly reduced tau spread and memory loss in rTg4510 mice.

222 of Ashwagandha (Withania somnifera) restores memory loss in scopolamine (SC)-induced mice.

223 The exact mechanisms leading to memory loss in tauopathies are not yet known; however, d

224 sults indicate that a substantial portion of memory loss in Tg2576 mice is not permanent.

225 ignificant, gradually progressive short-term memory loss in the absence of any history of strokes or

226 prenatal hypoxia on hippocampal atrophy and memory loss in the adult offspring.

227 s into new therapeutic strategies for curing memory loss in the disease.

228 of the beta-amyloid peptide (Abeta)-induced memory loss in the Drosophila brain.

229 y lead to an effective strategy for treating memory loss in the early stages of AD.

230 nd novel object recognition tests, and their memory loss in the novel object recognition test is asso

231 However, the molecular basis of memory loss in these mice is poorly understood.

232 endent deficits were eliminated, we detected memory loss in transgenic mice expressing mutant APP (Tg

233 Thus, NE stimulation may prevent memory loss in Ts65Dn mice, and may hold promise for tre

234 Thus, the clinical defects of learning and memory loss in vivo in GPI(-/-) PrP tg mice infected wit

235 are thought to instigate synapse damage and memory loss, induce depressive-like behavior in mice.

236 health complications include neurotoxicity, memory loss, infertility in males, and development of a

237 decline was similar in both families: early memory loss (initially selective for verbal memory in so

238 ography (FDG-PET) associated with short-term memory loss, insomnia, and temporal lobe electrographic

239 Memory loss is an early symptom of Alzheimer's Disease (

240 rain decline, yet it remains unclear whether memory loss is exacerbated beyond what atrophy alone wou

241 Temporally graded memory loss is interpreted traditionally as evidence for

242 fect of targeting miR-17 on AD pathology and memory loss is not clear.

243 nt attempts to describe those people in whom memory loss is not of such severity to merit a diagnosis

244 Age-related memory loss is observed across multiple mammalian specie

245 Memory loss is one of the most tragic symptoms of Alzhei

246 Memory loss is primarily caused by the accumulation of b

247 Memory loss is the signature feature of Alzheimer's dise

248 Acute alcohol-induced memory loss is thought to occur via inhibition of NMDA r

249 relationship between these two proteins and memory loss is unclear.

250 sruption of neural activity can also lead to memory loss, it may be that memory permanence is mediate

251 ghts into the molecular basis of age-related memory loss may hold promise for new treatments for cogn

252 complaints but without dementia or isolated memory loss (mean follow-up 31 months).

253 al events, including any neurological event, memory loss, movement disorders, and other neurological

254 observed associations of TDP-43 with greater memory loss, naming and functional decline, and smaller

255 The latter, hippocampal-dependent memory loss occurred in the absence of long-term potenti

256 mory deficits similar to FDD(KI/+) mice, and memory loss of FDD(KI/+) mice is prevented by expression

257 d memory defects in young flies but enhances memory loss of older flies.

258 ovelty exposure prevented the stress-induced memory loss of the spatial task and increased BDNF and A

259 complaints, 21 patients with severe isolated memory loss of unknown cause were identified and followe

260 ovel view of the effects of tau and Abeta on memory loss, offering new therapeutic opportunities in t

261 s first priority for patients suffering from memory loss or Alzheimer's disease (AD).

262 CI 1.2-3.6; p=0.008) and limitations due to memory loss or confusion (PR 5.8, 1.5-22.4; p=0.010) wer

263 omen, 14 men) with difficult-to-characterize memory loss or dementia (using standard clinical criteri

264 is, which leads to permanent brain injuries, memory loss or even death.

265 e of side effects such as impaired movement, memory loss, or epileptic seizures.

266 in reversal water maze learning, and little memory loss over time.

267 teristic features of Alzheimer's disease are memory loss, plaques resulting from abnormal processing

268 l, Trem1 haploinsufficiency prevents spatial memory loss, preserves homeostatic microglial morphology

269 ral atrophy has previously been described as memory loss, prosopagnosia, getting lost and behavioural

270 and how they are compromised in age-related memory loss remain hypothetical.

271 Profound and persistent memory loss resulting from insult to the hippocampus in

272 Profound and persistent memory loss resulting from insult to the hippocampus in

273 lso experience devastating features, such as memory loss, seizures and stroke.

274 erative disorder associated with progressive memory loss, severe dementia, and hallmark neuropatholog

275 Longitudinal studies of age-related memory loss should include genetic risk and subjective m

276 e neurodegenerative disorder with associated memory loss, spatial disorientation, and other psychiatr

277 minent epigenetic modification linked to the memory loss symptoms associated with neurodegenerative d

278 Memory loss, synaptic dysfunction, and accumulation of a

279 ppeared to have resulted in a greater object memory loss than early hippocampal lesions.

280 ercentage of subjects experience age-related memory loss that burdens daily performance.

281 s the trilogy mainly responsible for causing memory loss that has now been documented for over 20 yea

282 imer's disease (AD) research is the cause of memory loss that leads to dementia.

283 , thus determining a more or less pronounced memory loss (the leakage).

284 aging and Alzheimer disease and may lead to memory loss through disruption of medial temporal lobe (

285 ht arise from active mechanisms that promote memory loss to achieve various functions, such as minimi

286 eimer's disease While the findings show that memory loss usually exceeds executive dysfunction in pat

287 By preventing measles-associated immune memory loss, vaccination protects polymicrobial herd imm

288 Time-related memory loss varied greatly from food to food.

289 sexecutive symptoms; and for three patients, memory loss was accompanied by apathy but no other behav

290 oss was the only complaint; for one patient, memory loss was accompanied by personality change; for t

291 ied by personality change; for two patients, memory loss was accompanied by prominent dysexecutive sy

292 Concussion involving memory loss was also associated with a greater risk of c

293 For two patients, memory loss was the only complaint; for one patient, mem

294 ical and molecular mechanisms of age-related memory loss, we assessed spatial memory in C57BL/B6 mice

295 a colloid cyst, a condition associated with memory loss when accompanied by fornix and/or mammillary

296 eneralization to a novel environment show no memory loss when the hippocampus is subsequently inactiv

297 tion, accumulation of lipofuscin bodies, and memory loss, whereas their cortical and hippocampal neur

298 y many PD patients, including depression and memory loss, which do not respond well to currently avai

299 2050 and the problems caused by age-related memory loss will be dramatically aggravated.

300 ports from an informant that the patient has memory loss yields an LR of 6.5 (95% CI, 4.4-9.6) for de