Cyclerion Therapeutics (CYCN) 8-K On a mission to develop treatments that restore cognitive function CORPORATE PRESENTATION

Exhibit 99.1

 On a mission to develop treatments that restore cognitive function  CORPORATE PRESENTATION 

 Safe harbor statement  This document contains forward-looking statements within the meaning of Section 27A of the Securities Act of 1933, as amended, and Section 21E of the Securities Exchange Act of 1934, as amended.Our forward-looking statements are based on current beliefs and expectations of our management team that involve risks, potential changes in circumstances, assumptions, and uncertainties, including statements about the anticipated timing of release of topline results of our clinical trials; the progression of our discovery programs into clinical development; and the business and operations of the Company. We may, in some cases use terms such as “predicts,” “believes,” “potential,” “continue,” “anticipates,” “estimates,” “expects,” “plans,” “intends,” “may,” “could,” “might,” “likely,” “will,” “should” or other words that convey uncertainty of the future events or outcomes to identify these forward-looking statements. Each forward-looking statement is subject to risks and uncertainties that could cause actual results to differ materially from those expressed or implied in such statement. Applicable risks and uncertainties include those related to the possibility that any results of operations and financial condition of the Company reported are preliminary and subject to final audit and the risks listed under the heading “Risk Factors” and elsewhere in our 2020 Form 10-K filed on February 25, 2021, and our subsequent SEC filings. Investors are cautioned not to place undue reliance on these forward-looking statements. These forward-looking statements (except as otherwise noted) speak only as of the date of this report, and the Company undertakes no obligation to update these forward-looking statements, except as required by law. 

 On a mission to develop treatments that restore cognitive function      Tapping into a fundamental CNS signaling pathway with CY6463, a first-in-class, CNS-penetrant sGC stimulator  Executing biomarker-guided development strategy in well-defined populations with cognitive impairment  Tackling the enormous burden and breadth of cognitive impairment through an innovative portfolio of indications and molecules   

    Contents  NO-sGC-cGMP is a fundamental CNS signaling pathway  CY6463 translational pharmacology clinical study results  Advancing next-generation sGC stimulator program   Pipeline centered around improving cognitive function  Potential for patient impact: 3 studies underway  Executing on our priorities 

 NO-sGC-cGMP is a fundamental CNS signaling pathway    

 CY6463 amplifies the fundamental NO-sGC-cGMP signaling pathway    CY6463First-in-class BBB-permeable, positive allosteric modulator of sGCAmplifies endogenous NO-sGC-CGMP signaling to address central aspects of disease pathophysiology  Preclinical data and extensive academic work validate the crucial role of the NO-sGC-cGMP pathway in brain physiology  Synaptic plasticity  Neuro-inflammation  Bioenergetics  Vascular function  PKG, PDE, ion channels  Downstream targets (e.g., CREB, BDNF)  Important role in learning and memory     

   CY6463 improves endpoints relevant to cognition    Young Control   Aged Control   Aged CY6463   R6/2 + CY6463 46 nM  R6/2 + CY6463 7 nM  R6/2  WT  Morphological plasticity  In-vivo learning and memory  Ex-vivo LTP  Young rat/Vehicle  Aged rat/Vehicle  Aged rat/CY6463  Young rat/Vehicle  Aged rat/Vehicle  Aged rat/CY6463    *p<0.05 vs. the aged control group 

 CY6463 amplifies a fundamental CNS signaling pathway  NO-sGC-cGMP pathway plays a critical role in brain functionsGC stimulation with CY6463 amplifies NO-sGC-cGMP signalingMorphological, ex vivo and in vivo data demonstrate important role of sGC in synaptic plasticity, learning and memory, and 6463’s ability to restore deficits in these endpoints   

 CY6463 Translational Pharmacology Study Results 

   CY6463 showed rapid and persistent improvements in multiple independent biomarkers associated with cognitive impairment    In a 15-day study in 24 healthy elderly subjects CY6463 demonstrated:   Increased alpha and gamma power  Improved N200 latency  Faster saccadic eye movement (SEM) reaction time  Reduced neuroinflammatory biomarkers  Rapid onset (<15 days) Effect increased with ageBiomarkers linked to AD and aging   

 Phase 1b translational pharmacology study designed to evaluate CNS activity  *due to COVID restrictions, 12 subjects completed only period 1  Healthy elderly population (≥65 years)  Objectives  washout  CY6463 QD  CY6463 QD  Placebo  Placebo  15 days  15 days  24 subjects completed period 1  12 subjects completed both periods*  Safety and tolerabilityPharmacokinetics  Target engagementCNS activity  

   CY6463 showed rapid improvement in biomarkers of cognition    Increased alpha and gamma power  Faster saccadic eye movement reaction time  Improved N200 latency    Alpha power: CY6463 vs. placebo    Day 15  Improvement    Age (years)  Untreated    CY6463 treated    Time (ms)      Time (sec)  p=0.0216  Placebo  CY6463  p=0.0216    Improvement  0.02  0.00  -0.02  -0.04      Reduced neuroinflammatory biomarkers  In a 15-day study in 24 healthy elderly subjects, CY6463 demonstrated:  

 Pipeline centered around improving cognitive Function    

   CY6463 data point to potential in cognition    Preclinical CNS pharmacology  Potential to improve cognitive function  Neuronal function  Neuro-inflammation  Bioenergetics  Vascular function          Increased posterior alpha and gamma power  Improved N200 latency  Faster saccadic eye movement (SEM) andreaction time  Reduced neuroinflammatory biomarkers in CSF        Clinical CNS pharmacology*      *In a 15-day study in 24 healthy elderly subjects 

   Cognitive impairment is a debilitating facet of many CNS diseases  Neurodegenerative  Alzheimer’s Disease   Parkinson’s Dementia   Lewy Body Dementia   Neuropsychiatric      Major Depressive Disorder  Bipolar Disorder   Autism   Cancer/chemotherapy-induced cognitive impairment  Traumatic brain injury  Stroke  Event-related  Mitochondrial    Leigh Syndrome  Kearns-Sayre Syndrome  ADv  ongoing  CIAS   ongoing  MELAS  ongoing  ~2M  ~35M  ~13M  ~5M  Orphan  Orphan  Orphan  ~21M  ~150M  ~27M  ~10M  ~21M (US)  ~12M  ~5M (US)  Represents approximate prevalence of patients with cognitive impairment associated with other CNS diseases, worldwide in millions, except where noted as US prevalence  References on file.  

   Biomarker-guided development strategy in well-defined populations with cognitive impairment  ADv | Alzheimer’s Disease with vascular pathology (ADv) CIAS | Cognitive Impairment Associated with SchizophreniaMELAS | Mitochondrial Encephalomyopathy, Lactic Acidosis, and Stroke-like episodes  MELAS  ADv  Neurodegenerative      Parallel studies in distinct populations  Efficient, signal-seeking studies inform larger and longer studies  Disease-relevant biomarkers accelerate and guide development       Improving Cognition   Neuropsychiatric  CIAS  Mitochondrial Disease  Significant additional opportunities   Translation of insights across programs increases odds of success   

 Potential for patient impact: our priority indications 

     DISCOVERY  IND-ENABLING  PHASE 1*  PHASE 1b/2a  PHASE 2  CY6463  MELAS              ADv              CIAS              Multiple under assessment             CY3018   Multiple under assessment                       Advancing parallel, signal-seeking, exploratory studies in priority patient populations  *Two phase 1 studies were completed in healthy young and old (>65 years of age) volunteers confirming targeted CNS exposure and activity 

   Growing patient population, devastating impact, limited treatments  Biomarker-guided development strategy: ADv  Exploratory Phase 2Near-term impact on disease-specific biomarkers and cognition  Larger, longer studies symptomatic trialsfocused on cognition Initial approval expected on surrogate, symptomatic or functional endpoints  Standard of carefor patients with ADv Potential for disease modification and expansion into broader AD  Today  Tomorrow  Future          Alzheimer’sDisease  VascularDementia        ADv 

 ADv study ongoing  20  Exploratory, signal-seeking study to evaluate safety, tolerability, and pharmacodynamic effects (EEG, MRI, neuroinflammatory biomarkers, cognition)  Once-daily CY6463 vs. placebo12 weeks30 participants  Confirmed AD pathology (PET, CSF)2+ cardiovascular risk factorsMild-moderate subcortical small-vessel disease on MRIMini mental state exam score (20-26)  Objectives  Study design  Patient targeting   Partially funded by the Alzheimer's Association’s Part the Cloud-Gates Partnership Collaborating with Dr. Andrew Budson at Boston University on a study to examine the relationship between ERP/EEG and cognitive measures in dementias   Collaborations 

 Biomarker-guided development strategy: MELAS  Exploratory Phase 2Near-term impact ondisease-specific biomarkers   Larger, longer symptomatic trials focused on cognition and stroke-like-episodes Potential for accelerated approvalwith predictive biomarker  Transformative therapy for patients with MELAS Potential for expansion into additional mitochondrial diseases  Today  Tomorrow  Future          MELAS is a serious orphan disease, with significant CNS impact, no approved treatments  

 MELAS study ongoing; data expected 1H 2022   22  Objectives  Exploratory, signal-seeking study to evaluate safety, tolerability, and pharmacodynamic effects (MRI, biomarkers)  Study design  29-day open label Once-daily CY6463Up to 20 adults (targeting 12 completers)  Patient targeting   Genetically confirmed mitochondrial disease with neurological features of MELAS Elevated plasma lactate (disease biomarker)  Sites and collaborations  Study performed at centers of excellence for mitochondrial medicine: CHOP, MGH, Children’s National Hospital, Columbia University, Johns Hopkins University Preclinical collaboration with Dr. Marni Falk at CHOP to elucidate the role of sGC in mitochondrial disease models 

 Biomarker-guided development strategy: CIAS  Exploratory Phase 1bSafety + near-term impact on disease-relevant biomarkers   Larger, longer studies focused on biomarker-identified populations  Standard of care adjunctive therapy Improve cognitive impairment and functional outcomes  Today  Tomorrow  Future          CIAS is a debilitating and untreated facet of schizophrenia, with large and growing unmet need 

 CIAS study ongoing  24  Objectives  Exploratory, signal-seeking study to evaluate safety, tolerability, and pharmacodynamic effects (qEEG, ERP, digital cognitive performance battery)  Study design  14-day in clinic, randomized, placebo-controlled, double-blinded Once-daily CY6463Approximately 60 participants across sequential cohorts  Patient targeting   Psychiatrically stable adults with schizophreniaOn stable antipsychotic regimen 

 Next generation sGC stimulator program 

 Next generation sGC stimulator CY3018: selectively targeting the CNS   Greater relative CNS exposure  Greater relative CNS pharmacology  Greater CSF:plasma ratio for CY3018 translating into greater relative CNS pharmacologyCY3018 is progressing though IND-enabling developmentOngoing pharmacology studies to validate amenable CNS indications  CY3018  Data displayed as mean+ SEM, Relative pharmacology ratio: 1-hour post-dose with vehicle-subtraction 

 Executing on our priorities 

 2021: executing on our priorities  28  * Preliminary, unaudited unrestricted cash, cash equivalents and restricted cash balance as of March 31, 2021  Clinical andpre-clinical   ADv Ph2 study ongoingMELAS Ph2 study data expected H1 2022CIAS Ph1b study ongoingAdvancing CY3018, next-generation development candidate  Partnerships  Explore CNS collaborationsPraliciguat out-license complete   Capabilities and capital   Grow external CNS network and augment coreteam CNS expertiseReduced monthly cash use to ~50% that of 2020Q2 2021 ending cash balance of ~$70M 

 On a mission to develop treatments that restore cognitive function      Tapping into a fundamental CNS signaling pathway with CY6463, a first-in-class, CNS-penetrant sGC stimulator  Executing biomarker-guided development strategy in well-defined populations with cognitive impairment  Tackling the enormous burden and breadth of cognitive impairment through an innovative portfolio of indications and molecules   

 Appendices  Preclinical, Phase 1 and translational pharmacology studies, references 

 Preclinical Data    

   CY6463 demonstrated beneficial effects in preclinical studies across multiple domains associated with cognitive disease   32      Cerebral Blood FlowIncreased blood flow in areas associated with memory and arousal by fMRI BOLD imaging   IMPROVED      CellularBioenergeticsIncreased ATP and restored gene expression in cells from patients with mitochondrial diseases  ENHANCED    Neuronal FunctionEnhanced memory & spine density in aged animals; increased LTP in neurodegenerative models; affected qEEG spectra  IMPROVED    Neuro- inflammationDecreased markers of LPS-induced neuroinflammation (ICAM1, VCAM1, IL6) in vitro  REDUCED 

 CY6463 improved neuronal function  Restored hippocampal long-term potentiation to wild-type levels in a mouse neurodegenerative model    Wild type  Disease    Disease + CY6463 (46 nM)  *    Normalized fEPSPAmplitude  Time (min)  10  30  50  70  1.0  5  2.0  2.5  ImproveNeuronal Function  ReduceNeuroinflammation  EnhanceCellular Bioenergetics  ImproveCerebral Blood Flow  Hippocampal slices from symptomatic Huntington’s Disease (R6/2) mice incubated with CY6463 for 25-30 minutes before LTP inductionExtracellular field potentials recordings performed using Multi-Electrode Array; **p<0.01 vs. Disease  By acting directlyon the neurons,CY6463 could restore impaired neurotransmission 

 CY6463 increased qEEG gamma power   No effect seen with PDE9 inhibitor  Healthy awake rats were treated with clinically relevant doses of CY6463 (3 mg/kg) or PDE9 inhibitor (10 mg/kg) Graph displays 1-2h post-dose, mean ± SEM  ImproveNeuronal Function  ReduceNeuroinflammation  EnhanceCellular Bioenergetics  ImproveCerebral Blood Flow  CY6463 isdifferentiated from PDE9 inhibitor, which showed no effect on gamma power    Gamma Power  Vehicle  PDE9i  CY6463  CY6463 + PDE9i 

 CY6463 and donepezil act independently to enhance qEEG signal  Combination elicited additive increase in gamma band power in healthy rats  ImproveNeuronal Function  ReduceNeuroinflammation  EnhanceCellular Bioenergetics  ImproveCerebral Blood Flow  *p<0.05 vs Veh# p<0.05 CY6463 vs CY6463 +DonepezilHealthy rats orally administered CY6463 (10mg/kg), Donepezil (1mg/kg), or a combination. Graph displays 1-2h post-dose, mean ± SEM  CY6463 may offer opportunity to enhance attention and cognitive performance alone and on top of standard of care      Gamma Power  Vehicle  Donepezil  CY6463  CY6463 + Donepezil 

   CY6463 improved learning and memory in aged rats  Increased rate of learning in aged rats treated with CY6463 in Morris Water Maze  Healthy aged male rats were administered CY6463 (10 mg/kg, p.o.) daily during Morris Water Maze training  Young rat/Vehicle  Aged rat/Vehicle  Aged rat/CY6463  Young rat/Vehicle  Aged rat/Vehicle  Aged rat/CY6463  *p<0.05 vs. Aged vehicle-treated  ImproveNeuronal Function  ReduceNeuroinflammation  EnhanceCellular Bioenergetics  ImproveCerebral Blood Flow     

   CY6463 improved cognitive function in pharmacologically impaired rats  ImproveNeuronal Function  ReduceNeuroinflammation  EnhanceCellular Bioenergetics  ImproveCerebral Blood Flow  Rat Novel Object Recognition    *p<0.05 vs. VEH + MK-801 rats   CY6463 acts downstream of NMDA receptor to reverse deficit induced by NMDA antagonist (MK-801) 

 Mushroom spine density  Restoration of spine density has potential to provide neuroprotectiveeffects and improve synaptic function in neurodegenerative diseases    CY6463 improved neuronal function   Enhanced hippocampal spine density in aged animals treated with CY6463    Young Control   Aged Control   Aged CY6463   Control   Young   CY6463  Control   Aged        *  *  ImproveNeuronal Function  ReduceNeuroinflammation  EnhanceCellular Bioenergetics  ImproveCerebral Blood Flow  *p<0.05 vs. Aged3-month old (young) or 16-month old (aged) healthy mice at study initiationAged mice treated for 4 months with 1 mg/kg CY6463 

   CY6463 reduced neuroinflammation  Inhibited in vitro LPS-induction of biomarkers of neuroinflammation  39    *p<0.05 vs. control LPS-treated wellsCY6463 (10 µM) and DETA (30 µM) were incubated with SIM-A9 cells or rat brain 3D microtissues for 30 minutes before LPS (100 ng/ml) incubation and further incubated for 18-20h at 37oC before IL-6 quantification in the media  Neuroinflammation in mouse microglial cells  Neuroinflammation in rat brain 3D microtissues    *  ImproveNeuronal Function  ReduceNeuroinflammation  EnhanceCellular Bioenergetics  ImproveCerebral Blood Flow          CY6463  Control  Control  CY6463  Control  Control  *  * 

 CY6463 enhanced cellular bioenergetics  Increased ATP and restored decreased gene expression in cells from patients with mitochondrial diseases  40  *p<0.05 vs. vehicle-treated wellsGM13740 Leigh Syndrome patient cells obtained from the Coriell Institute were treated for 24h before ATP quantificationTFAM: mitochondrial transcriptional factor A, a key activator of mitochondrial transcription as well as a participant in mitochondrial genome replication.  ImproveNeuronal Function  ReduceNeuroinflammation  EnhanceCellular Bioenergetics  ImproveCerebral Blood Flow      TFAM  Mitochondrial disease patient cells  *  *  *  * 

   CY6463 improved cerebral blood flow  41            Increased blood flow in areas associated with memory and arousal by fMRI BOLD imaging   Peripherally restricted sGC stimulator  CNS-penetrant sGC stimulator CY6463  Reticular activating system  Thalamus  Cortical transition areas  Ventral hippocampus  ImproveNeuronal Function  ReduceNeuroinflammation  EnhanceCellular Bioenergetics  ImproveCerebral Blood Flow  Healthy awake male rats treated with 0.3 mg/kg iv; image quantification 20-30 minutes post-dose  

 Phase 1 study results    

           Results    CY6463 phase 1 showed CNS exposure, target engagement, PK, and safety    PHASE 1 (completed)        110 healthy young  Age range 18-63  Standard safety  Identified safe and well-tolerated dose levels with steady-state CNS exposure in therapeutic target range*  Linear, predictable PK, consistentwith QD dosing  CNS exposure confirmed  Evidence of target engagement(blood pressure)  GoalsAchieved  Study designThree stages:  SAD  MAD  Food Interaction          PK (blood & CSF)  Wide dose range tested      Well tolerated at all dose levels,no safety signals  May be taken with or without food  *Based on positive CNS pharmacology in multiple preclinical models 

 Translational Pharmacology Study Results    

   CY6463 showed rapid and persistent improvements in multiple independent biomarkers associated with cognitive impairment    In a 15-day study in 24 healthy elderly subjects CY6463 demonstrated:   Increased alpha and gamma power  Improved N200 latency  Faster saccadic eye movement (SEM) reaction time  Reduction in neuroinflammatory biomarkers  Rapid onset (<15 days) Effect increased with ageBiomarkers linked to AD and aging   

 Biomarker overview: qEEG frequency bands and their clinical implications  qEEG is quantitative electroencephalography, an objective method that measures electrical activity and brain wave patterns    Resting-state qEEG: subjects sit facing a featureless wall without movingrecorded with eyes open and closed for 5 minutes each  Band  Frequency Hz  associated with   Delta  0-4  Deep sleep  Theta  4-8  Waking/falling asleep, some with cognition  Alpha  8-14  Passive wakefulnessAttention and cognitive processing  Beta  14-30  Alert, concentration  Gamma  30-80  Higher cognitive function  Associated with: Cognitive decline in aging and ADGenetic risk factors for AD (ApoE4)AD pathological protein levels (Aβ, tau)Improvement with approved AD treatments   

 CY6463 improved qEEG measures: significant increase in alpha power  qEEG is quantitative electroencephalography, an objective method that measures electrical activity and brain wave patterns        CY6463 vs. baseline  Significant increase in EEG alpha power  No effect of placebo  Placebo vs. baseline  CY6463 vs. placebo  change (%) in alpha power on day 15 

 CY6463’s consistent alpha power effects across repeat sessions indicate stable and robust signal  Footer  DAY 1baseline  DAY 15change from baseline  CY6463 relative to placebo  CY6463  Placebo  Pre-dose 1  Pre-dose 2  Pre-doselast dose  2 hr post-dose  3 hr post-dose  6 hr post-dose      Magnitude of improvement equivalent to decline seen after 2 years of aging 

   CY6463 increased alpha power with high responder rate (>70%)  1. Includes all subjects. For CY6463 and pbo each: n=12 for period 1, n=6 for period 2  Increase in alpha powerDay 15 change from baseline in mean closed-eye alpha (8-12 Hz) Power  Consistent individual treatment responsesPosterior Closed-Eye Alpha (8-12 Hz) Power  Placebo  CY6463  Placebo  CY6463  Posterior  p = 0.0197  %  17% treatment effect over placeboSimilar increase in anterior alpha power observed (p=0.0752)  13/18 participants increase with CY6463, vs 5/18 with placebo1Overall effect not driven by outliers  Placebo  CY6463  BL  BL  D15  D15 

 CY6463 treatment associated with trend improvement in gamma power    Change in Closed-Eye Gamma (25-45 Hz) Power  Placebo  CY6463  Placebo  CY6463    200  150  100  50  0  -50  -100  Anterior (p = 0.081)  Posterior (p = 0.1163)  Change from baseline (%) 

 Biomarker overview: event-related potential (ERP)    Trial: 500 tones80% standard, 20% deviant                          Deviant    Standard  ERP oddball paradigmSubjects wear EEG cap and headphones, hear tones with instruction to press a button upon deviant tones    P300  N200    N200Stable component of ERP waveformStimulus identification and distinctionAffected in aging, neurodegenerative and neuropsychiatric diseases with cognitive impairment, and other CNS diseases  ParametersLatency: time after the stimulus to peak signalAmplitude: size of peak signal 

 CY6463 improved N200 latency and effect increased with age    Day 15  Improvement    Age (years)  Untreated    CY6463 treated    Time (ms)    Effect of age on N200 latency    Overall decrease in N200 latency for CY6463 treated vs untreated on day 15 (p<0.02)  Effect more pronouncedin older subjects   

 65 to 69yn=10  ≥70 yn=14  p=0.016    CY6463 improved N200 latency, driven byresponse in older subjects  Greater decrease in ≥70y vs <70yDay 15 change from baseline    Latency response was greater in subjects ≥70y vs 65-69y (p=0.016)  Narrowing of variance in ≥ 70y supports a drug effect    In ≥ 70y, magnitude of improvement after 2 weeks of treatment with CY6463 represents ~10y age-related change in N200 latency  Time (ms)  3.0  1.5  0.0  1.5 

   Biomarker overview: saccadic eye movement as an objective measure of attention and cognition    Short, fast, simultaneous tracking of both eyes in the same direction   Brain areas involved include the frontal cortex, superior colliculus, substantia nigra, and amygdala    Considered to be reflective of attention / arousal and influenced by motivation, time on task, and task difficulty    Sensitive to sedation, fatigue, and CNS depressants and cognitive enhancers, and is affected by aging  Peak Velocity    Amplitude  Latency  Duration  T=0ms        Eye Position  Eye Velocity            https://www.liverpool.ac.uk/~pcknox/teaching/Eymovs/params.htm 

 CY6463 improved saccadic eye movement, an objective functional measure  Decrease in saccadic reaction time  Increase in saccadic peak velocity  Shorter saccadic reaction times and faster saccadic velocities indicate that CY6463 is improving CNS functional performance – motor output – in addition to CNS neurophysiologyCognitive enhancers (e.g., modafinil) also positively impact saccadic eye movements  Time (sec)  p=0.0216  Placebo  CY6463  Placebo  CY6463  p=0.0216  p=0.07    Improvement    Velocity (deg/sec)  Improvement  Mean change from baseline on day 15 post-dose  0.02  0.00  -0.02  -0.04  150  100  50  0 

         CY6463 improved neuroinflammatory biomarkers    A2M and C3 are associated with pathological aging and Alzheimer’s Disease     Alpha-2-macroglobulin (A2M) levels predict cognitive decline and development of AD; may lead to tau hyperphosphorylation    Complement C3 (C3) colocalizes with Aβ plaques and tau tangles; involved in synaptic remodeling and degeneration        LS % Mean Difference from placebo at Day 15 (95% CI)   

 Relevant reference publications    

 Relevant reference publications (1 of 2)  NO-sGC-cGMP signaling in the CNSCorreia S, et al. “The CNS-penetrant soluble guanylate cyclase stimulators CY6463 reveals its therapeutic potential in neurodegenerative diseases.” Frontiers in Pharmacology. 2021;12(1014)Correia S, et al. “The CNS-penetrant soluble guanylate cyclase stimulators CYR119 attenuates markers of inflammation in the central nervous system.” Journal of Neuroinflammation. 2021;18(1)Garthwaite, John. “Nitric oxide as a multimodal brain transmitter.” Brain and Neuroscience Advances vol. 2 2398212818810683.4 Dec. 2018 Kleppisch T, Feil R. cGMP signaling in the mammalian brain: role in synaptic plasticity and behaviour. Handb Exp Pharmacol. 2009;(191):549-79Ben Aissa M, Lee SH, Bennett BM, Thatcher GR. Targeting NO/cGMP Signaling in the CNS for Neurodegeneration and Alzheimer's Disease. Curr Med Chem. 2016;23(24):2770-2788Hollas MA, Ben Aissa M, Lee SH, Gordon-Blake JM, Thatcher GRJ. Pharmacological manipulation of cGMP and NO/cGMP in CNS drug discovery. Nitric Oxide. 2019 Jan 1;82:59-74qEEG spectral frequency analysisIshii et al. Healthy and Pathological Brain Aging: From the Perspective of Oscillations, Functional Connectivity, and Signal Complexity. Neuropsychobiology, 2018Babiloni, et al. Resting-state posterior alpha rhythms are abnormal in subjective memory complaint seniors with preclinical Alzheimer's neuropathology and high education level: the INSIGHT-preAD study. Neurobiol Aging. 2020;90:43-59 

 Relevant reference publications (2 of 2)  Event-related potential (ERP): MMN, N200 and P300Bennys K, Portet F, Touchon J. Diagnostic value of event-related evoked potentials N200 and P300 subcomponents in early diagnosis of Alzheimer’s disease and mild cognitive impairment. J Clin Neurophysiol 2007;24:405–12Fruehwirt et al. Associations of event-related brain potentials and Alzheimer’s disease severity: A longitudinal study. Progress in Neuropsychopharmacology and Biological Psychiatry 92 (2019) 31-38Saccadic eye movement (SEM)Wilcockson et al. Abnormalities of saccadic eye movements in dementia due to Alzheimer’s disease and mild cognitive impairment. Aging 2019, Vol.11, No.15James A. Sharpe & David H. Zackon (1987) Senescent Saccades: Effects of Aging on Their Accuracy, Latency and Velocity, Acta Oto-Laryngologica, 104:5-6, 422-428ADvCortes-Canteli M, Iadecola C. Alzheimer’s Disease and Vascular Aging: JACC Focus Seminar. J Am Coll Cardiol. 2020;75(8):942-951MELASEl-Hattab AW, Adesina AM, Jones J, Scaglia F. MELAS syndrome: Clinical manifestations, pathogenesis, and treatment options. Mol Genet Metab. 2015;116(1-2):4-12CIASKeefe RS, Harvey PD. Cognitive impairment in schizophrenia. Handb Exp Pharmacol. 2012;(213):11-37