Neurodegenerative disease is characterized by the loss of neurons or myelin in the brain and spinal cord, deteriorating over time and leading to dysfunction.6, 7 The brain and spinal cord comprise neurons that have different functions, such as controlling motion, processing sensory information, and making decisions. The cells of the brain and spinal cord are generally not regenerated; thus, excessive damage can be devastating and irreversible. Neurodegenerative diseases are widespread worldwide. The long course and lack of effective treatment of these diseases impose a heavy burden on individuals, families, and society. In recent years, many studies have shown that lncRNA can participate in the regulation of neurodegenerative disease occurrence and development. Based on existing research results, this paper focuses on lncRNA in several common neurodegenerative diseases. We made a summary of lncRNAs involved in this review (Table 1).Table 1Dysregulated lncRNAs in Neurodegenerative DiseaseslncRNAsDescriptionAssociated DiseaseCulprit or BodyguardBiological FunctionBACE1-AStranscribe from the antisense protein-coding BACE 1 geneADculpritbind to BACE1 and increase the stability of its mRNA, thereby promoting the synthesis of BACE1 protein, and further increase the production of Aβ of cellsBC200homologous with rodent BC1 lncRNA; the earliest specific example showed lncRNAs conservationADculpritinduce APP mRNA translation via association with FMRP and then aggregate the accumulation of Aβ in the brain17Aembedded in the human G-protein-coupled receptor 51 geneADculpritimpair GABAB signaling pathway by decreasing GABAB R2 transcriptionNAT-Rad18transcribed from the antisense of protein coding gene Rad18ADculpritdown the expression of DNA repair protein Rad18 and enhance susceptibility to neuronal apoptosis51Aan antisense transcript of intron 1 of the SORL1 geneADculpritaltering the spliced form of SORL1 mRNA and resulting in Aβ42 accumulationGDNFOStranscribed from the opposite strand of GDNF geneADculpritnegatively regulate the expression of GDNFHttAS_v1antisense transcript of the Htt geneHDbodyguardreduce endogenous HTT transcript levelsBDNFOSantisense transcription product of BDNFHDbodyguardupregulates the transcription of BDNF and have a protective effect on neuronsNEAT1a nuclear-enriched ncRNA essential for the formation and maintenance of paraspecklesHDbodyguardessential for the integrity of the nuclear paraspeckle substructure; increase viability under oxidative stressHAR1F and HAR1Rantisense transcripts of the first HAR1 geneHDbodyguardinvolved in neurotransmission, memory structure, and synaptic plasticity in the mature brainDGCR5a transcript of DiGeorge critical region 5HDbodyguardinclude a genome binding site for REST and play an important transcriptional regulatory role in HDMEG3the human homolog of the mouse maternally expressed gene Gtl2, the first imprinted gene identified on the mouse distal chromosome 12HDculpritalter gene expression in response to neuronal activityABHD11-AS1homologous with rodent Abhd11os lncRNAHDbodyguardattenuate the toxicity of Htt mRNANaPINK1transcribed from the antisense of PINK1 locusPDbodyguardstabilize PINK1 expressionAS Uchl1antisense transcript of Uchl1PDbodyguardregulate the expression of UCHL1 at the post-transcriptional level, thus promoting the translation process and increasing protein synthesisHOTAIRantisense intergenic RNA transcribed from the HOXC locusPDculpritincrease the stability of LRRK2 mRNA and upregulated its expression, thus inducing DA neuronal apoptosisMALAT1also known as NEAT2 and is a highly conserved ncRNA highly expressed in neuronsPDculpritupregulate a-synuclein expression, thus driving the pathogenesis of PD