Rescue of cognitive-aging by administration of a neurogenic and/or neurotrophic compound

  title={Rescue of cognitive-aging by administration of a neurogenic and/or neurotrophic compound},
  author={Silvia Bolognin and Mario Buffelli and Jukka T. Puoliv{\"a}li and Khalid Iqbal},
  journal={Neurobiology of Aging},
Elevated Tau Level in Aged Rat Cerebrospinal Fluid Reduced by Treatment with a Neurotrophic Compound.
The therapeutic potential of P021 as a disease-modifying compound and the suitability of the aged Fisher rats as a model of cerebral aging in which the therapeutic efficacy of a tau-reducing compound can be monitored in the CSF are shown.
Prevention of dendritic and synaptic deficits and cognitive impairment with a neurotrophic compound
Availability of appropriate neurotrophic support during the period of synaptic compensation can prevent synaptic deficit and cognitive impairment, and P021 is a promising neurotrophic compound for this purpose.
Neurotrophic Treatment Initiated During Early Postnatal Development Prevents the Alzheimer-Like Behavior and Synaptic Dysfunction
Findings indicate that treatment with the neurotrophic peptide mimetic such as P021 during early development can be an effective therapeutic strategy to rescue synaptic deficit and cognitive impairment in familial AD and related tauopathies.
N-Acetyl Transferase, Shati/Nat8l, in the Dorsal Hippocampus Suppresses Aging-induced Impairment of Cognitive Function in Mice.
A reduction in Shati/Nat8l mRNA expression in the dorsal hippocampus of mice as a result of their aging is observed, and decreased N-acetyl aspartate (NAA) in aged mice was upregulated by Shatin8l overexpression, suggesting that the Shati-Nat8L-NAA pathway determines cognitive function with aging.
Innovative Therapy for Alzheimer’s Disease-With Focus on Biodelivery of NGF
The intent of this review is describing available experimental and clinical data related to AD therapy, priming to gain additional facts associated with the importance of NGF for AD treatment, and encapsulated cell biodelivery (ECB) as an efficient tool for NGF delivery.
Prevention of Amyloid-β and Tau Pathologies, Associated Neurodegeneration, and Cognitive Deficit by Early Treatment with a Neurotrophic Compound.
P021 treatment initiated during the synaptic compensation period can prevent neurodegeneration, Aβ and tau pathologies, rescue episodic memory impairment, and markedly reduce mortality rate, suggesting that improving the health of the neuronal network can prevent AD.
Prenatal to early postnatal neurotrophic treatment prevents Alzheimer-like behavior and pathology in mice
Investigating for the first time the effect of oral treatment during prenatal to early postnatal development with a neurotrophic compound, P021, on neurobehavior and AD-like pathology in 3xTg-AD, a transgenic mouse model of AD, suggests that neurotrophic impairment during early development can be one of the etiopathogenic factors of AD.


Pharmacologic reversal of neurogenic and neuroplastic abnormalities and cognitive impairments without affecting Aβ and tau pathologies in 3xTg-AD mice
Peripheral administration of Peptide 6, an 11-mer, which makes an active region of ciliary neurotrophic factor (CNTF, amino acid residues 146–156), restored cognition by enhancing neurogenesis and neuronal plasticity in these mice.
Age-related memory decline is associated with vascular and microglial degeneration in aged rats
Beneficial effect of a CNTF tetrapeptide on adult hippocampal neurogenesis, neuronal plasticity, and spatial memory in mice.
Peptide 6c treatment improved encoding of hippocampal-dependent information in a spatial reference memory task in mice and demonstrated the therapeutic potential of Peptides 6c for regeneration of the brain and improvement of cognition.
The aging hippocampus: A multi-level analysis in the rat
Impact of aging on hippocampal function: plasticity, network dynamics, and cognition
Linking Redox Regulation of NMDAR Synaptic Function to Cognitive Decline during Aging
Evidence is provided for a link between the redox-mediated decline in NMDAR function and emergence of an age-related cognitive phenotype, impairment in the rapid acquisition and retention of novel spatial information.
An experimental rat model of sporadic Alzheimer’s disease and rescue of cognitive impairment with a neurotrophic peptide
Peripheral administration of Peptide 6 rescued neurodegeneration and cognitive deficit in I2NTF–CTF animals by increasing dentate gyrus neurogenesis and mRNA level of brain derived neurotrophic factor.
Neurogenesis in a rat model of age‐related cognitive decline
It is demonstrated that aged rats that maintain cognitive function do so despite pronounced reductions in hippocampal neurogenesis, and the interesting possibility that impaired hippocampal function is associated with greater survival of newly generated hippocampal neurons at advanced ages is suggested.