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Alcohol-induced brain damage can also result in memory defects and a major decline in intellectual abilities and social skills (see alcoholism).
Interestingly, transgenic overexpression or central administration of the potentially amyloidogenic C99 fragments has been reported to induce memory defects and neurodegeneration [45], [46], [47], [48], [49].
These conflicting results have prompted us to further examine the relationship between ventricular size and neurobehavioural deficits (locomotive, learning and memory defects), and to investigate the morphological changes observed in rats with experimental hydrocephalus.
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Alzheimer's disease (AD), the most common neurodegenerative disease among the elderly, is characterized by synaptic and memory defects, neuroinflammation, and progressive neuronal death.
Transgenic mice overexpressing human or mouse Dyrk1A have been generated and were shown to display hippocampal-dependent spatial learning and memory defects, developmental delay and motor deficits [90].
The critical role of T3 and TTR in hippocampal development and function is further demonstrated by the findings that prenatal and neonatal hypothyroidism cause learning and memory defects, including mental retardation in children (Zoeller and Rovet, 2004).
We have previously shown that expression of the human Aβ42 peptide in Drosophila brains induces age-dependent memory defects, locomotor dysfunction, and neurodegeneration accompanied by Aβ42 deposits [14].
In the mouse FXS model, minocycline promoted the maturation of hippocampal dendritic spines towards normal morphology, both in vitro and in vivo, and repressed anxiety and memory defects in an elevated plus-maze test (Bilousova et al., 2009).
Induced loss of FGF signaling only in postnatal astrocytes generates stereotypic locomotor hyperactivity and learning and memory defects that correlate with deficit in specific cell populations in the postnatal brain (Müller Smith et al, 2008, Stevens et al, 2012).
Thus, we sought to determine if Reelin treatment could recover the synaptic plasticity and learning and memory defects observed in the AS mouse model.
Our previous studies demonstrate that adeno-assocated virus transfection of the adult AS mouse model with a UBE3A construct could significantly ameliorate the synaptic plasticity and learning and memory defects (Daily et al., 2011).
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