Aging and age-associated cognitive impairments are complex and multifactorial and involve both genetic as well as environmental determinants. Both in humans and in animal models the process of normal aging often results in cognitive decline, with or without the presence of any aging Homatropine Bromide related neurological disorders. Disorders related to cognitive impairments range from non-syndromic benign senescent forgetfulness to the syndromic memory loss that characterizes Alzheimer’s disease. These manifestations are highly heterogeneous and individual, family, and population specific. They continue to increase with the current trend in longevity in most populations. As such they are Atractylenolide-III emerging as a major societal challenge. Attempts in the last decade to gain insight into aging and age-associated learning impairments have been aided by advances in genome-wide methods and technologies, particularly gene expression involving microarrays. Further, the hippocampus in the brain is integral to memory function including spatial memory both in humans and in rodents. It is greatly affected by aging, and is among the first to be affected during dementia. The microarray technology has been used widely, more specifically, to understand the gene expression changes related to aging and age-associated memory impairments in the hippocampus in humans using post-mortem tissues and in animal models such as rodents after behavioural training. Results show that learning induces a complex reprogramming of gene expression, which is also affected by the aging processes. Moreover, the results of the individual studies are heterogeneous and often difficult to interpret. They often highlight different gene sets and pathways, have limited conclusions, and do not consider their broader implications that may go beyond individual experiments. It is therefore desirable to integrate results from these studies towards a consensus view of the genes affected and the molecular mechanisms underlying brain aging and age-associated learning impairments. This is now possible because of the availability of considerable amount of original microarray data in the public microarray data repositories, as well as the availability of improved statistical analytical methods. This study focuses on age-associated spatial learning impairment. It uses original results from all available microarray gene expression data involving ASLI in rats using an inverse-variance meta-analysis approach. The results establish that a large number of genes are differentially expressed across age and across spatial learning impairment. More importantly, they allow identification of pertinent lists of aging and ASLI related genes. Further, the follow up analysis has offered a novel insight into the underlying molecular pathways associated with aging and age-related non-syndromic memory impairments such as ASLI. For network analysis the mapped identifiers were overlaid onto a global molecular network developed from information contained in the IPA Knowledge Base. Networks of network eligible molecules were then algorithmically generated based on their connectivity. Next, the functional analysis of a network identified the biological functions and/or diseases that were most significant to the molecules in the network based on the association of the network molecules with the biological functions and/or diseases in the Ingenuity Knowledge Base. Right-tailed Fisher’s exact test was used to calculate a p-value determining the probability that each biological function and/or disease assigned to that network is due to chance alone. Canonical pathways analysis identified the pathways from the IPA library of canonical pathways that were most significant to the gene lists.